Review



rabbit polyclonal antibody against fmdv vp1 protein  (Bioss)


Bioz Verified Symbol Bioss is a verified supplier
Bioz Manufacturer Symbol Bioss manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 94
      Buy from Supplier

    Structured Review

    Bioss rabbit polyclonal antibody against fmdv vp1 protein
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Polyclonal Antibody Against Fmdv Vp1 Protein, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pmc13157663-48-79-97?v=Bioss
    Average 94 stars, based on 3 article reviews
    rabbit polyclonal antibody against fmdv vp1 protein - by Bioz Stars, 2026-08
    94/100 stars

    Images

    1) Product Images from "Mechanistic role of lipid metabolism in foot-and-mouth disease virus (FMDV) replication"

    Article Title: Mechanistic role of lipid metabolism in foot-and-mouth disease virus (FMDV) replication

    Journal: Veterinary Research

    doi: 10.1186/s13567-026-01762-6

    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV VP1 protein.
    Figure Legend Snippet: The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV VP1 protein.

    Techniques Used: Staining, Labeling, Infection, Quantitative RT-PCR, Western Blot, Viral Plaque Assay, Expressing

    The effect of FASN on FMDV replication. A BHK-21 cells were treated with 30 μM C75, 75 μM palmitic acid, or 30 μM C75 plus 75 μM palmitic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–45 μM C75 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of C75. D RT–qPCR confirmed that C75 treatment inhibits FMDV replication. E Western blot analysis verified that C75 treatment suppresses the expression of FMDV VP1 protein. F Combined treatment with 10 μM C75 and TOFA exerted a stronger inhibitory effect on FMDV replication. G Viral plaque assay demonstrated that C75 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–75 μM palmitic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 30 μM C75, supplementation with 0–75 μM palmitic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM C75, addition of 75 μM palmitic acid partially rescued FMDV VP1 protein expression. K BHK-21 cells were treated with 5–30 μM 2-bromopalmitate (2‑BP) for 24 h, and cell viability was not significantly affected. L RT–qPCR confirmed that 2‑BP treatment inhibits FMDV replication. M Western blot analysis verified that 2‑BP treatment suppresses the expression of FMDV VP1 protein.
    Figure Legend Snippet: The effect of FASN on FMDV replication. A BHK-21 cells were treated with 30 μM C75, 75 μM palmitic acid, or 30 μM C75 plus 75 μM palmitic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–45 μM C75 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of C75. D RT–qPCR confirmed that C75 treatment inhibits FMDV replication. E Western blot analysis verified that C75 treatment suppresses the expression of FMDV VP1 protein. F Combined treatment with 10 μM C75 and TOFA exerted a stronger inhibitory effect on FMDV replication. G Viral plaque assay demonstrated that C75 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–75 μM palmitic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 30 μM C75, supplementation with 0–75 μM palmitic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM C75, addition of 75 μM palmitic acid partially rescued FMDV VP1 protein expression. K BHK-21 cells were treated with 5–30 μM 2-bromopalmitate (2‑BP) for 24 h, and cell viability was not significantly affected. L RT–qPCR confirmed that 2‑BP treatment inhibits FMDV replication. M Western blot analysis verified that 2‑BP treatment suppresses the expression of FMDV VP1 protein.

    Techniques Used: Staining, Infection, Quantitative RT-PCR, Western Blot, Expressing, Viral Plaque Assay

    The effect of LDs on FMDV replication. A BHK-21 cells were treated with 30 μM A922500, 60 μM oleic acid, or 30 μM A922500 plus 60 μM oleic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–60 μM A922500 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of A922500. D A922500 inhibited FMDV replication by 50% (EC 50 ) at 11.86 μM. E RT–qPCR confirmed that A922500 treatment inhibits FMDV replication. F Western blot analysis verified that A922500 treatment suppresses FMDV VP1 protein expression. G Viral plaque assay demonstrated that A922500 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–120 μM oleic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 15 μM A922500, supplementation with 0–75 μM oleic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM A922500, addition of 60 μM oleic acid partially rescued FMDV VP1 protein expression.
    Figure Legend Snippet: The effect of LDs on FMDV replication. A BHK-21 cells were treated with 30 μM A922500, 60 μM oleic acid, or 30 μM A922500 plus 60 μM oleic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–60 μM A922500 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of A922500. D A922500 inhibited FMDV replication by 50% (EC 50 ) at 11.86 μM. E RT–qPCR confirmed that A922500 treatment inhibits FMDV replication. F Western blot analysis verified that A922500 treatment suppresses FMDV VP1 protein expression. G Viral plaque assay demonstrated that A922500 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–120 μM oleic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 15 μM A922500, supplementation with 0–75 μM oleic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM A922500, addition of 60 μM oleic acid partially rescued FMDV VP1 protein expression.

    Techniques Used: Staining, Infection, Quantitative RT-PCR, Western Blot, Expressing, Viral Plaque Assay



    Similar Products

    rabbit polyclonal antibody against fmdv vp1 protein  (Bioss)
    94
    Bioss rabbit polyclonal antibody against fmdv vp1 protein
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Polyclonal Antibody Against Fmdv Vp1 Protein, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pmc13157663-48-79-97?v=Bioss
    Average 94 stars, based on 1 article reviews
    rabbit polyclonal antibody against fmdv vp1 protein - by Bioz Stars, 2026-08
    94/100 stars
    		  Buy from Supplier
    rabbit polyclonal igg antibodies against p tau181  (Signalway Antibody)
    86
    Signalway Antibody rabbit polyclonal igg antibodies against p tau181
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Polyclonal Igg Antibodies Against P Tau181, supplied by Signalway Antibody, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pm42271186-97-35-59?v=Signalway+Antibody
    Average 86 stars, based on 1 article reviews
    rabbit polyclonal igg antibodies against p tau181 - by Bioz Stars, 2026-08
    86/100 stars
    		  Buy from Supplier
    rabbit polyclonal antibodies against hdc  (Progen Biotechnik)
    86
    Progen Biotechnik rabbit polyclonal antibodies against hdc
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Polyclonal Antibodies Against Hdc, supplied by Progen Biotechnik, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pm42276055-296-6-14?v=Progen+Biotechnik
    Average 86 stars, based on 1 article reviews
    rabbit polyclonal antibodies against hdc - by Bioz Stars, 2026-08
    86/100 stars
    		  Buy from Supplier
    rabbit polyclonal antibody against p38γ  (OriGene)
    92
    OriGene rabbit polyclonal antibody against p38γ
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Polyclonal Antibody Against P38γ, supplied by OriGene, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pm42201586-60-14-21?v=OriGene
    Average 92 stars, based on 1 article reviews
    rabbit polyclonal antibody against p38γ - by Bioz Stars, 2026-08
    92/100 stars
    		  Buy from Supplier
    rabbit monoclonal antibody against human cd34  (OriGene)
    94
    OriGene rabbit monoclonal antibody against human cd34
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Monoclonal Antibody Against Human Cd34, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pm42167651-55-5-15?v=OriGene
    Average 94 stars, based on 1 article reviews
    rabbit monoclonal antibody against human cd34 - by Bioz Stars, 2026-08
    94/100 stars
    		  Buy from Supplier
    custom rabbit polyclonal antibody against crtc2 p ser433  (Huabio Inc)
    86
    Huabio Inc custom rabbit polyclonal antibody against crtc2 p ser433
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Custom Rabbit Polyclonal Antibody Against Crtc2 P Ser433, supplied by Huabio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pm42151152-538-1-11?v=Huabio+Inc
    Average 86 stars, based on 1 article reviews
    custom rabbit polyclonal antibody against crtc2 p ser433 - by Bioz Stars, 2026-08
    86/100 stars
    		  Buy from Supplier
    antibodies against s100  (OriGene)
    94
    OriGene antibodies against s100
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Antibodies Against S100, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pm42103358-115-8-11?v=OriGene
    Average 94 stars, based on 1 article reviews
    antibodies against s100 - by Bioz Stars, 2026-08
    94/100 stars
    		  Buy from Supplier
    rabbit polyclonal antibody against inos  (Bioss)
    94
    Bioss rabbit polyclonal antibody against inos
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Polyclonal Antibody Against Inos, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/10__1186_slash_s41936___026___00580___8-88-19-24?v=Bioss
    Average 94 stars, based on 1 article reviews
    rabbit polyclonal antibody against inos - by Bioz Stars, 2026-08
    94/100 stars
    		  Buy from Supplier
    rabbit polyclonal antibody against phospho hif 1α  (Abmart Inc)
    86
    Abmart Inc rabbit polyclonal antibody against phospho hif 1α
    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV <t>VP1</t> protein.
    Rabbit Polyclonal Antibody Against Phospho Hif 1α, supplied by Abmart Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pm42037413-75-0-11?v=Abmart+Inc
    Average 86 stars, based on 1 article reviews
    rabbit polyclonal antibody against phospho hif 1α - by Bioz Stars, 2026-08
    86/100 stars
    		  Buy from Supplier
    rabbit polyclonal antibody against rat tnf α  (Novus Biologicals)
    94
    Novus Biologicals rabbit polyclonal antibody against rat tnf α
    Schematic overview of the study design and experimental timeline. The surgery involved (1) an anterior abdominal approach, followed by (2) EP injury, and (3) intradiscal injection of <t>either</t> <t>TNF‐α</t> or C. acnes , such that all outcome measures reflect the combined effects of both the EP injury and the respective injectate. Pain‐like behavior was evaluated biweekly using the von Frey assay to assess hind paw mechanical allodynia. Post‐euthanasia assessments included ex vivo spinal MRI using T1w and T2w sequences as well as histological analysis of spine and spinal cord. The timeline depicts the three experimental cohorts and the corresponding analyses time points. C. acnes, Cutibacterium acnes ; EP, endplate; MRI, magnetic resonance imaging; T1w, T1‐weighted.
    Rabbit Polyclonal Antibody Against Rat Tnf α, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+rabbit+polyclonal/pmc13102498-115-18-27?v=Novus+Biologicals
    Average 94 stars, based on 1 article reviews
    rabbit polyclonal antibody against rat tnf α - by Bioz Stars, 2026-08
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV VP1 protein.

    Journal: Veterinary Research

    Article Title: Mechanistic role of lipid metabolism in foot-and-mouth disease virus (FMDV) replication

    doi: 10.1186/s13567-026-01762-6

    Figure Lengend Snippet: The effect of ACC on FMDV replication. A Research pathway map for de novo fatty acid synthesis. B BHK-21 cells were treated with 30 μM TOFA, 60 μM malonyl‑CoA, or 30 μM TOFA plus 60 μM malonyl‑CoA. After fixation, cells were stained with Nile red, and nuclei were labeled with DAPI (blue). Scale bar, 20 µm. C BHK-21 cells were treated with 5–45 μM TOFA for 24 h, and cell viability was not significantly affected. D Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of TOFA. E RT–qPCR confirmed that TOFA treatment inhibits FMDV replication. F Western blot analysis confirmed that TOFA treatment suppresses FMDV replication. G TOFA inhibited FMDV replication by 50% (EC 50 ) at 21.33 μM. H CP640186 inhibited FMDV replication by 50% (EC 50 ) at 0.2021 μM. I Viral plaque assay demonstrated that TOFA treatment significantly reduces FMDV replication. J BHK-21 cells were treated with 5–120 μM malonyl‑CoA for 24 h, and cell viability was not substantially affected. K RT–qPCR showed that, in the presence of 15 μM TOFA, supplementation with 0–45 μM malonyl‑CoA partially restored FMDV replication. L Western blot analysis confirmed that, in the presence of 45 μM TOFA, addition of 60 μM malonyl‑CoA partially rescued the expression of FMDV VP1 protein.

    Article Snippet: The hamster kidney fibroblasts (BHK-21) used in the experiments were purchased from Wuhan Punosai Life Science and Technology Co. Acetyl-CoA carboxylase inhibitor TOFA (HY-100568) was purchased from MedChemExpress (MCE); fatty acid synthase inhibitor C75 (HY-12364) was purchased from MCE; malonyl-CoA (HY-115899) was purchased from MCE; palmitic acid (HY-N0830) was purchased from MCE; DGAT-1 inhibitor A922500 (HY-10038) was purchased from MCE; oleic acid (HY-N1446) was purchased from MCE; CPT1A inhibitors Etomoxir (HY-50202) and CP640186 (HY-15259) were purchased from MCE; and rabbit polyclonal antibody against FMDV VP1 protein (type O) (bs-41049R) was purchased from Beijing Biosynthesis Biotechnology Co., Ltd. (bioss).

    Techniques: Staining, Labeling, Infection, Quantitative RT-PCR, Western Blot, Viral Plaque Assay, Expressing

    The effect of FASN on FMDV replication. A BHK-21 cells were treated with 30 μM C75, 75 μM palmitic acid, or 30 μM C75 plus 75 μM palmitic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–45 μM C75 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of C75. D RT–qPCR confirmed that C75 treatment inhibits FMDV replication. E Western blot analysis verified that C75 treatment suppresses the expression of FMDV VP1 protein. F Combined treatment with 10 μM C75 and TOFA exerted a stronger inhibitory effect on FMDV replication. G Viral plaque assay demonstrated that C75 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–75 μM palmitic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 30 μM C75, supplementation with 0–75 μM palmitic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM C75, addition of 75 μM palmitic acid partially rescued FMDV VP1 protein expression. K BHK-21 cells were treated with 5–30 μM 2-bromopalmitate (2‑BP) for 24 h, and cell viability was not significantly affected. L RT–qPCR confirmed that 2‑BP treatment inhibits FMDV replication. M Western blot analysis verified that 2‑BP treatment suppresses the expression of FMDV VP1 protein.

    Journal: Veterinary Research

    Article Title: Mechanistic role of lipid metabolism in foot-and-mouth disease virus (FMDV) replication

    doi: 10.1186/s13567-026-01762-6

    Figure Lengend Snippet: The effect of FASN on FMDV replication. A BHK-21 cells were treated with 30 μM C75, 75 μM palmitic acid, or 30 μM C75 plus 75 μM palmitic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–45 μM C75 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of C75. D RT–qPCR confirmed that C75 treatment inhibits FMDV replication. E Western blot analysis verified that C75 treatment suppresses the expression of FMDV VP1 protein. F Combined treatment with 10 μM C75 and TOFA exerted a stronger inhibitory effect on FMDV replication. G Viral plaque assay demonstrated that C75 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–75 μM palmitic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 30 μM C75, supplementation with 0–75 μM palmitic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM C75, addition of 75 μM palmitic acid partially rescued FMDV VP1 protein expression. K BHK-21 cells were treated with 5–30 μM 2-bromopalmitate (2‑BP) for 24 h, and cell viability was not significantly affected. L RT–qPCR confirmed that 2‑BP treatment inhibits FMDV replication. M Western blot analysis verified that 2‑BP treatment suppresses the expression of FMDV VP1 protein.

    Article Snippet: The hamster kidney fibroblasts (BHK-21) used in the experiments were purchased from Wuhan Punosai Life Science and Technology Co. Acetyl-CoA carboxylase inhibitor TOFA (HY-100568) was purchased from MedChemExpress (MCE); fatty acid synthase inhibitor C75 (HY-12364) was purchased from MCE; malonyl-CoA (HY-115899) was purchased from MCE; palmitic acid (HY-N0830) was purchased from MCE; DGAT-1 inhibitor A922500 (HY-10038) was purchased from MCE; oleic acid (HY-N1446) was purchased from MCE; CPT1A inhibitors Etomoxir (HY-50202) and CP640186 (HY-15259) were purchased from MCE; and rabbit polyclonal antibody against FMDV VP1 protein (type O) (bs-41049R) was purchased from Beijing Biosynthesis Biotechnology Co., Ltd. (bioss).

    Techniques: Staining, Infection, Quantitative RT-PCR, Western Blot, Expressing, Viral Plaque Assay

    The effect of LDs on FMDV replication. A BHK-21 cells were treated with 30 μM A922500, 60 μM oleic acid, or 30 μM A922500 plus 60 μM oleic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–60 μM A922500 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of A922500. D A922500 inhibited FMDV replication by 50% (EC 50 ) at 11.86 μM. E RT–qPCR confirmed that A922500 treatment inhibits FMDV replication. F Western blot analysis verified that A922500 treatment suppresses FMDV VP1 protein expression. G Viral plaque assay demonstrated that A922500 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–120 μM oleic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 15 μM A922500, supplementation with 0–75 μM oleic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM A922500, addition of 60 μM oleic acid partially rescued FMDV VP1 protein expression.

    Journal: Veterinary Research

    Article Title: Mechanistic role of lipid metabolism in foot-and-mouth disease virus (FMDV) replication

    doi: 10.1186/s13567-026-01762-6

    Figure Lengend Snippet: The effect of LDs on FMDV replication. A BHK-21 cells were treated with 30 μM A922500, 60 μM oleic acid, or 30 μM A922500 plus 60 μM oleic acid. After fixation, cells were stained with Nile red. Scale bar, 20 µm. B BHK-21 cells were treated with 5–60 μM A922500 for 24 h, and cell viability was not significantly affected. C Cytopathic effect (CPE) following FMDV infection in the presence of increasing concentrations of A922500. D A922500 inhibited FMDV replication by 50% (EC 50 ) at 11.86 μM. E RT–qPCR confirmed that A922500 treatment inhibits FMDV replication. F Western blot analysis verified that A922500 treatment suppresses FMDV VP1 protein expression. G Viral plaque assay demonstrated that A922500 treatment significantly inhibits FMDV replication. H BHK-21 cells were treated with 5–120 μM oleic acid for 24 h, and cell viability was not substantially affected. I RT–qPCR showed that, in the presence of 15 μM A922500, supplementation with 0–75 μM oleic acid partially restored FMDV replication. J Western blot analysis confirmed that, in the presence of 45 μM A922500, addition of 60 μM oleic acid partially rescued FMDV VP1 protein expression.

    Article Snippet: The hamster kidney fibroblasts (BHK-21) used in the experiments were purchased from Wuhan Punosai Life Science and Technology Co. Acetyl-CoA carboxylase inhibitor TOFA (HY-100568) was purchased from MedChemExpress (MCE); fatty acid synthase inhibitor C75 (HY-12364) was purchased from MCE; malonyl-CoA (HY-115899) was purchased from MCE; palmitic acid (HY-N0830) was purchased from MCE; DGAT-1 inhibitor A922500 (HY-10038) was purchased from MCE; oleic acid (HY-N1446) was purchased from MCE; CPT1A inhibitors Etomoxir (HY-50202) and CP640186 (HY-15259) were purchased from MCE; and rabbit polyclonal antibody against FMDV VP1 protein (type O) (bs-41049R) was purchased from Beijing Biosynthesis Biotechnology Co., Ltd. (bioss).

    Techniques: Staining, Infection, Quantitative RT-PCR, Western Blot, Expressing, Viral Plaque Assay

    Schematic overview of the study design and experimental timeline. The surgery involved (1) an anterior abdominal approach, followed by (2) EP injury, and (3) intradiscal injection of either TNF‐α or C. acnes , such that all outcome measures reflect the combined effects of both the EP injury and the respective injectate. Pain‐like behavior was evaluated biweekly using the von Frey assay to assess hind paw mechanical allodynia. Post‐euthanasia assessments included ex vivo spinal MRI using T1w and T2w sequences as well as histological analysis of spine and spinal cord. The timeline depicts the three experimental cohorts and the corresponding analyses time points. C. acnes, Cutibacterium acnes ; EP, endplate; MRI, magnetic resonance imaging; T1w, T1‐weighted.

    Journal: JOR Spine

    Article Title: Intradiscal Cutibacterium acnes Sustains Modic Type 1‐Like Lesions Over Time in a Rat Lumbar Endplate Injury Model

    doi: 10.1002/jsp2.70182

    Figure Lengend Snippet: Schematic overview of the study design and experimental timeline. The surgery involved (1) an anterior abdominal approach, followed by (2) EP injury, and (3) intradiscal injection of either TNF‐α or C. acnes , such that all outcome measures reflect the combined effects of both the EP injury and the respective injectate. Pain‐like behavior was evaluated biweekly using the von Frey assay to assess hind paw mechanical allodynia. Post‐euthanasia assessments included ex vivo spinal MRI using T1w and T2w sequences as well as histological analysis of spine and spinal cord. The timeline depicts the three experimental cohorts and the corresponding analyses time points. C. acnes, Cutibacterium acnes ; EP, endplate; MRI, magnetic resonance imaging; T1w, T1‐weighted.

    Article Snippet: Sections were then incubated for 1 h at room temperature with one of the following primary antibodies: (i) rabbit polyclonal antibody against rat TNF‐α (1:500 dilution, #NBP1‐19532, Novus Biologics, MN, USA), (ii) rabbit recombinant multiclonal antibody against rat NE (1:500 dilution, #ab314916, Abcam, Waltham, MA, USA), or (iii) rabbit recombinant polyclonal antibody against rat CD19 (1:150 dilution, #27949‐1‐AP, ThermoFisher, Waltham, MA, USA).

    Techniques: Injection, Ex Vivo, Magnetic Resonance Imaging

    Degree of disc degeneration was increased in both EP injury + C. acnes and EP injury + TNF‐α discs compared to Sham without difference between injury groups. (A) Representative T1w and T2w MRI of discs per group and timepoint. (B) Both EP injury + C. acnes and EP injury + TNF‐α discs were significantly more degenerated than Sham at 8‐ and 14 weeks post‐injury, with no differences between the two injury groups at any time point. Disc degeneration increased over time in the EP injury + C. acnes group. Bars represent median with IQR. Significance bars represent results of Tukey's post hoc analysis of pairwise comparisons after detecting main effects with a two‐way ANOVA. Timepoints week 1, 8, and 14: Sham: N = 8 discs, EP injury + TNF‐α: N = 12–14 discs, EP injury + C. acnes : N = 10–12 discs. (C) Representative histological images of whole discs per group and timepoint, SafO/F/H staining. (D) Quantification of histological disc degeneration score. Discs from both EP injury groups were significantly more degenerated than Sham at all‐time points (weeks 1, 8, and 14). No significant differences were observed between EP injury + TNF‐α versus EP injury + C. acnes groups at any time point. Bars represent median with IQR. Significance bars represent results of Tukey's post hoc analysis of pairwise comparisons after detecting main effects with a two‐way ANOVA. Timepoints week 1, 8, and 14: Sham: N = 6–7 discs, EP injury + TNF‐α: N = 10–12 discs, EP injury + C. acnes : N = 9–12 discs. ANOVA, analysis of variance; C. acnes , Cutibacterium acnes ; EP, endplate; IQR, interquartile range; SafO/F/H, Safranin‐O/fastgreen/hematoxylin; T1w, T1‐weighted.

    Journal: JOR Spine

    Article Title: Intradiscal Cutibacterium acnes Sustains Modic Type 1‐Like Lesions Over Time in a Rat Lumbar Endplate Injury Model

    doi: 10.1002/jsp2.70182

    Figure Lengend Snippet: Degree of disc degeneration was increased in both EP injury + C. acnes and EP injury + TNF‐α discs compared to Sham without difference between injury groups. (A) Representative T1w and T2w MRI of discs per group and timepoint. (B) Both EP injury + C. acnes and EP injury + TNF‐α discs were significantly more degenerated than Sham at 8‐ and 14 weeks post‐injury, with no differences between the two injury groups at any time point. Disc degeneration increased over time in the EP injury + C. acnes group. Bars represent median with IQR. Significance bars represent results of Tukey's post hoc analysis of pairwise comparisons after detecting main effects with a two‐way ANOVA. Timepoints week 1, 8, and 14: Sham: N = 8 discs, EP injury + TNF‐α: N = 12–14 discs, EP injury + C. acnes : N = 10–12 discs. (C) Representative histological images of whole discs per group and timepoint, SafO/F/H staining. (D) Quantification of histological disc degeneration score. Discs from both EP injury groups were significantly more degenerated than Sham at all‐time points (weeks 1, 8, and 14). No significant differences were observed between EP injury + TNF‐α versus EP injury + C. acnes groups at any time point. Bars represent median with IQR. Significance bars represent results of Tukey's post hoc analysis of pairwise comparisons after detecting main effects with a two‐way ANOVA. Timepoints week 1, 8, and 14: Sham: N = 6–7 discs, EP injury + TNF‐α: N = 10–12 discs, EP injury + C. acnes : N = 9–12 discs. ANOVA, analysis of variance; C. acnes , Cutibacterium acnes ; EP, endplate; IQR, interquartile range; SafO/F/H, Safranin‐O/fastgreen/hematoxylin; T1w, T1‐weighted.

    Article Snippet: Sections were then incubated for 1 h at room temperature with one of the following primary antibodies: (i) rabbit polyclonal antibody against rat TNF‐α (1:500 dilution, #NBP1‐19532, Novus Biologics, MN, USA), (ii) rabbit recombinant multiclonal antibody against rat NE (1:500 dilution, #ab314916, Abcam, Waltham, MA, USA), or (iii) rabbit recombinant polyclonal antibody against rat CD19 (1:150 dilution, #27949‐1‐AP, ThermoFisher, Waltham, MA, USA).

    Techniques: Staining

    Intradiscal injectate following EP injury determined MC subtype prevalence over time. (A) Representative T1w and T2w MR images showing MC1‐ (top), MC2‐ (middle), and MC3‐like (bottom) lesions in EP injury + TNF‐α (left) or EP injury + C. acnes (right) discs. All 3 different MC subtypes developed in both EP injury + TNF‐α and EP injury + C. acnes groups. MC1‐like lesions: T1w: Hypo‐, or isointense; T2w: Hyperintense. MC2‐like lesions: T1w and T2w: Hyperintense. MC3‐like lesions: T1w and T2w: Hypointense. Red arrows surround bone marrow lesions. Images are from time points 8‐ and 14‐weeks post‐injury. (B) Representative histological images of features associated with MC1 (cellular infiltrates), MC2 (fatty replacement of normal bone marrow), and MC3 (sclerotic bone) in EP injury + TNF‐α and EP injury + C. acnes groups. In both injury groups, all 3 histological features of MC subtypes were found. #: Normal bone marrow region. 1: Cellular infiltrates; 2: Fatty replacement of normal bone marrow; 3: Increased bone structure. SafO/F/H staining. (C) Quantification of MC1‐like lesion prevalence (% of total number of EPs: L6 cranial, L5 caudal, L5 cranial, L4 caudal) revealed that EP injury + intradiscal C. acnes injection resulted in a significantly higher prevalence of MC1‐like lesions across all 3 time points compared to both EP injury + TNF‐α and Sham. The EP injury + TNF‐α group tended to have significantly more MC1‐like lesions compared to Sham. (D) MC2‐like lesions increased in the EP injury + TNF‐α group over time and were significantly higher than EP injury + C. acnes and Sham at 14‐weeks post‐injury. (E) MC3‐like lesions increased over time in the EP injury + C. acnes group. Bars represent median with IQR. Significance bars represent pairwise comparisons from Tukey's post hoc analysis following two‐way ANOVA. Timepoints week 1, 8, and 14: Sham: N = 4 rats, EP injury + TNF‐α: N = 5–7 rats, EP injury + C. acnes : N = 5–6 rats. * p < 0.05, ** p < 0.01, *** p < 0.001. ANOVA, analysis of variance; C. acnes , Cutibacterium acnes ; EP, endplate; IQR, interquartile range; MC, modic change; SafO/F/H, Safranin‐O/fastgreen/hematoxylin; T1w, T1‐weighted.

    Journal: JOR Spine

    Article Title: Intradiscal Cutibacterium acnes Sustains Modic Type 1‐Like Lesions Over Time in a Rat Lumbar Endplate Injury Model

    doi: 10.1002/jsp2.70182

    Figure Lengend Snippet: Intradiscal injectate following EP injury determined MC subtype prevalence over time. (A) Representative T1w and T2w MR images showing MC1‐ (top), MC2‐ (middle), and MC3‐like (bottom) lesions in EP injury + TNF‐α (left) or EP injury + C. acnes (right) discs. All 3 different MC subtypes developed in both EP injury + TNF‐α and EP injury + C. acnes groups. MC1‐like lesions: T1w: Hypo‐, or isointense; T2w: Hyperintense. MC2‐like lesions: T1w and T2w: Hyperintense. MC3‐like lesions: T1w and T2w: Hypointense. Red arrows surround bone marrow lesions. Images are from time points 8‐ and 14‐weeks post‐injury. (B) Representative histological images of features associated with MC1 (cellular infiltrates), MC2 (fatty replacement of normal bone marrow), and MC3 (sclerotic bone) in EP injury + TNF‐α and EP injury + C. acnes groups. In both injury groups, all 3 histological features of MC subtypes were found. #: Normal bone marrow region. 1: Cellular infiltrates; 2: Fatty replacement of normal bone marrow; 3: Increased bone structure. SafO/F/H staining. (C) Quantification of MC1‐like lesion prevalence (% of total number of EPs: L6 cranial, L5 caudal, L5 cranial, L4 caudal) revealed that EP injury + intradiscal C. acnes injection resulted in a significantly higher prevalence of MC1‐like lesions across all 3 time points compared to both EP injury + TNF‐α and Sham. The EP injury + TNF‐α group tended to have significantly more MC1‐like lesions compared to Sham. (D) MC2‐like lesions increased in the EP injury + TNF‐α group over time and were significantly higher than EP injury + C. acnes and Sham at 14‐weeks post‐injury. (E) MC3‐like lesions increased over time in the EP injury + C. acnes group. Bars represent median with IQR. Significance bars represent pairwise comparisons from Tukey's post hoc analysis following two‐way ANOVA. Timepoints week 1, 8, and 14: Sham: N = 4 rats, EP injury + TNF‐α: N = 5–7 rats, EP injury + C. acnes : N = 5–6 rats. * p < 0.05, ** p < 0.01, *** p < 0.001. ANOVA, analysis of variance; C. acnes , Cutibacterium acnes ; EP, endplate; IQR, interquartile range; MC, modic change; SafO/F/H, Safranin‐O/fastgreen/hematoxylin; T1w, T1‐weighted.

    Article Snippet: Sections were then incubated for 1 h at room temperature with one of the following primary antibodies: (i) rabbit polyclonal antibody against rat TNF‐α (1:500 dilution, #NBP1‐19532, Novus Biologics, MN, USA), (ii) rabbit recombinant multiclonal antibody against rat NE (1:500 dilution, #ab314916, Abcam, Waltham, MA, USA), or (iii) rabbit recombinant polyclonal antibody against rat CD19 (1:150 dilution, #27949‐1‐AP, ThermoFisher, Waltham, MA, USA).

    Techniques: Staining, Injection

    Intradiscal C. acnes versus TNF‐α injection following EP injury determined adjacent bone marrow lesion immune cell response. (A) Representative images of intradiscal inflammatory burden measured as TNF‐α‐ir in Sham (left), TNF‐α (middle) and C. acnes (right)‐injected discs. Upper right images represent magnified areas of the overview section. Arrows indicate TNF‐α positive cells. (B) Both EP injury + TNF‐α and EP injury + C. acnes groups led to increased discal TNF‐α‐ir at all 3 time points without a difference between injury groups. Bars represent median with IQR. Significance bars represent pairwise comparisons from Tukey's post hoc analysis. Timepoints week 1, 8, and 14: Sham: N = 6–8 discs, EP injury + TNF‐α: N = 8–10 discs, EP injury + C. acnes : 10–12 discs. (C) Representative images of NE‐ir (top) and CD19‐ir (bottom). Red arrows indicate NE‐positive cells, orange arrows indicate CD19‐positive cells. (D) Bone marrow lesions adjacent to EP injury + C. acnes ‐ versus EP injury + TNF‐α‐ discs showed increased NE‐ir and CD19‐ir. Bars represent median with IQR. Significance bars represent results from Mann–Whitney U ‐test. All time points combined: EP injury + TNF‐α: N = 12 bone marrow lesions, EP injury + C. acnes : N = 16 bone marrow lesions. * p < 0.05, ** p < 0.01, *** p < 0.001. C. acnes , Cutibacterium acnes ; IQR, interquartile range; NE, neutrophil elastase.

    Journal: JOR Spine

    Article Title: Intradiscal Cutibacterium acnes Sustains Modic Type 1‐Like Lesions Over Time in a Rat Lumbar Endplate Injury Model

    doi: 10.1002/jsp2.70182

    Figure Lengend Snippet: Intradiscal C. acnes versus TNF‐α injection following EP injury determined adjacent bone marrow lesion immune cell response. (A) Representative images of intradiscal inflammatory burden measured as TNF‐α‐ir in Sham (left), TNF‐α (middle) and C. acnes (right)‐injected discs. Upper right images represent magnified areas of the overview section. Arrows indicate TNF‐α positive cells. (B) Both EP injury + TNF‐α and EP injury + C. acnes groups led to increased discal TNF‐α‐ir at all 3 time points without a difference between injury groups. Bars represent median with IQR. Significance bars represent pairwise comparisons from Tukey's post hoc analysis. Timepoints week 1, 8, and 14: Sham: N = 6–8 discs, EP injury + TNF‐α: N = 8–10 discs, EP injury + C. acnes : 10–12 discs. (C) Representative images of NE‐ir (top) and CD19‐ir (bottom). Red arrows indicate NE‐positive cells, orange arrows indicate CD19‐positive cells. (D) Bone marrow lesions adjacent to EP injury + C. acnes ‐ versus EP injury + TNF‐α‐ discs showed increased NE‐ir and CD19‐ir. Bars represent median with IQR. Significance bars represent results from Mann–Whitney U ‐test. All time points combined: EP injury + TNF‐α: N = 12 bone marrow lesions, EP injury + C. acnes : N = 16 bone marrow lesions. * p < 0.05, ** p < 0.01, *** p < 0.001. C. acnes , Cutibacterium acnes ; IQR, interquartile range; NE, neutrophil elastase.

    Article Snippet: Sections were then incubated for 1 h at room temperature with one of the following primary antibodies: (i) rabbit polyclonal antibody against rat TNF‐α (1:500 dilution, #NBP1‐19532, Novus Biologics, MN, USA), (ii) rabbit recombinant multiclonal antibody against rat NE (1:500 dilution, #ab314916, Abcam, Waltham, MA, USA), or (iii) rabbit recombinant polyclonal antibody against rat CD19 (1:150 dilution, #27949‐1‐AP, ThermoFisher, Waltham, MA, USA).

    Techniques: Injection, MANN-WHITNEY

    Pain‐like behavior and spinal cord sensitization was increased in both EP injury groups and SubP was significantly higher in the EP injury + C. acnes group. (A) Normalized hind paw withdrawal thresholds (% baseline) measured using von Frey testing over 13 weeks following EP injury with TNF‐α (blue squares) or C. acnes (pink triangles) injection, or sham surgery (black circles). Both EP injury groups demonstrated a significant and sustained reduction in mechanical thresholds compared to Sham, indicating long‐lasting mechanical hypersensitivity. No significant difference was observed between the EP injury + TNF‐α and EP injury + C. acnes groups. Data are shown as mean ± SD. Mixed‐effect analysis with Tukey post hoc analysis. * p < 0.05 for EP injury + TNF‐α versus Sham; # p < 0.05 for EP injury + C. acnes versus Sham. Time points 1–13 weeks: Sham: N = 4–12 rats, EP injury + TNF‐α: 6–19 rats, EP injury + C. acnes : 6–18 rats. (B) Random forest model showed that MC1‐like presence and area contributed strongest to pain‐like behavior. Graph shows %IncMSE. p values are FDR‐adjusted permutation‐based values. Black bars: p < 0.05. (C) Representative images of SubP expression spinal cord dorsal horn. (D) Quantification of SubP‐ir in the spinal cord dorsal horn area at 1‐, 8‐, and 14‐weeks. SubP levels were significantly increased in EP injury + TNF‐α and EP injury + C. acnes groups compared to Sham at 8‐ and 14‐weeks. SubP was significantly higher in EP injury + C. acnes versus EP injury + TNF‐α groups at 14‐WKs post‐injury. Significance bars represent results from Tukey's post hoc analysis. Time points weeks 1, 8, 14: Sham: N = 4, EP injury + TNF‐α: N = 6–7, EP injury + C. acnes : N = 5–6 spinal cords. (E) Representative images of GFAP expression in spinal cord dorsal horn. (F) Quantification of GFAP‐ir in the spinal cord dorsal horn area at 1‐, 8‐, and 14‐weeks. GFAP expression increased significantly in both EP injury + TNF‐α and EP injury + C . acnes groups compared to Sham, with a progressive increase from week 1 to week 14. There was no difference between injury groups. Significance bars represent results from Tukey post hoc analysis. Time points weeks 1, 8, 14: Sham: N = 4, EP injury + TNF‐α: N = 6–7, EP injury + C. acnes : N = 5–6. Bars represent mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001. C. acnes , Cutibacterium acnes ; EP, endplate; GFAP, glial fibrillary acidic protein; IncMSE, percent increase in mean standard error; IQR, interquartile range; MC, modic change; SubP, substance P.

    Journal: JOR Spine

    Article Title: Intradiscal Cutibacterium acnes Sustains Modic Type 1‐Like Lesions Over Time in a Rat Lumbar Endplate Injury Model

    doi: 10.1002/jsp2.70182

    Figure Lengend Snippet: Pain‐like behavior and spinal cord sensitization was increased in both EP injury groups and SubP was significantly higher in the EP injury + C. acnes group. (A) Normalized hind paw withdrawal thresholds (% baseline) measured using von Frey testing over 13 weeks following EP injury with TNF‐α (blue squares) or C. acnes (pink triangles) injection, or sham surgery (black circles). Both EP injury groups demonstrated a significant and sustained reduction in mechanical thresholds compared to Sham, indicating long‐lasting mechanical hypersensitivity. No significant difference was observed between the EP injury + TNF‐α and EP injury + C. acnes groups. Data are shown as mean ± SD. Mixed‐effect analysis with Tukey post hoc analysis. * p < 0.05 for EP injury + TNF‐α versus Sham; # p < 0.05 for EP injury + C. acnes versus Sham. Time points 1–13 weeks: Sham: N = 4–12 rats, EP injury + TNF‐α: 6–19 rats, EP injury + C. acnes : 6–18 rats. (B) Random forest model showed that MC1‐like presence and area contributed strongest to pain‐like behavior. Graph shows %IncMSE. p values are FDR‐adjusted permutation‐based values. Black bars: p < 0.05. (C) Representative images of SubP expression spinal cord dorsal horn. (D) Quantification of SubP‐ir in the spinal cord dorsal horn area at 1‐, 8‐, and 14‐weeks. SubP levels were significantly increased in EP injury + TNF‐α and EP injury + C. acnes groups compared to Sham at 8‐ and 14‐weeks. SubP was significantly higher in EP injury + C. acnes versus EP injury + TNF‐α groups at 14‐WKs post‐injury. Significance bars represent results from Tukey's post hoc analysis. Time points weeks 1, 8, 14: Sham: N = 4, EP injury + TNF‐α: N = 6–7, EP injury + C. acnes : N = 5–6 spinal cords. (E) Representative images of GFAP expression in spinal cord dorsal horn. (F) Quantification of GFAP‐ir in the spinal cord dorsal horn area at 1‐, 8‐, and 14‐weeks. GFAP expression increased significantly in both EP injury + TNF‐α and EP injury + C . acnes groups compared to Sham, with a progressive increase from week 1 to week 14. There was no difference between injury groups. Significance bars represent results from Tukey post hoc analysis. Time points weeks 1, 8, 14: Sham: N = 4, EP injury + TNF‐α: N = 6–7, EP injury + C. acnes : N = 5–6. Bars represent mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001. C. acnes , Cutibacterium acnes ; EP, endplate; GFAP, glial fibrillary acidic protein; IncMSE, percent increase in mean standard error; IQR, interquartile range; MC, modic change; SubP, substance P.

    Article Snippet: Sections were then incubated for 1 h at room temperature with one of the following primary antibodies: (i) rabbit polyclonal antibody against rat TNF‐α (1:500 dilution, #NBP1‐19532, Novus Biologics, MN, USA), (ii) rabbit recombinant multiclonal antibody against rat NE (1:500 dilution, #ab314916, Abcam, Waltham, MA, USA), or (iii) rabbit recombinant polyclonal antibody against rat CD19 (1:150 dilution, #27949‐1‐AP, ThermoFisher, Waltham, MA, USA).

    Techniques: Injection, Expressing