Review

ccl9 (R&D Systems)

Name: ccl9
Brand: R&D Systems
Rating: 93 (8 reviews)

R&D Systems is a verified supplier

R&D Systems manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

R&D Systems ccl9
Ccl9, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ccl9/product/R&D Systems
Average 93 stars, based on 8 article reviews

ccl9 - by Bioz Stars, 2026-02

93/100 stars

Images

Image Search Results

( A – E ) Detection of the uptake of B10F10-GFP by I-NCMs in vitro ( A – C ) and in vivo ( D and E ). Experimental design ( A ) and uptake of B16F10-GFP by RFP-labeled splenic ( B ) or blood ( C ) I-NCMs at 36 hours following coculture. The GFP signal in I-NCMs was detected by flow cytometry ( B ) or ICC ( C ). Monocytes and B16 cells were cocultured at a ratio of 5:1. White and yellow scale bars: 100 and 10 μm, respectively, in C . Experimental design ( D ) and FACS detection of uptake of B16F10-GFP materials by monocyte subsets in blood ( E , left) or lung (right) in Nr4a1 –/– mice after retro-orbital injection of MDP and B16F10-GFP injection. ( F – K ) I-NCMs recruit NK cells through CCL6 release to sites of B16F10 melanoma metastasis. ( F and G ) Adoptive transfer of I-NCMs ( F ) and MDP treatment ( G ) increased NK cells in the lungs of B16F10-bearing Nod2 –/– and Nr4a1 –/– mice, respectively. ( H ) MDP-triggered attenuation of B16F10 colonization in Nr4a1 –/– mice was inhibited by depletion of NK cells using NK1.1 antibody. ( I ) Bulk RNA-Seq data showing higher expression of Ccl6 and Ccl9 , but not other detected chemokine genes, in I-NCMs. ( J ) Anti-CCL6 antibody reduced NK cells and ( K ) suppressed the MDP-mediated attenuation of B16F10 colonization in Nr4a1 –/– mice. Data are presented as mean ± SEM; n = 4–10 in each group; * P < 0.05, ** P < 0.01, *** P < 0.001; 2-tailed t test in F and J , Kruskal-Wallis test in H , and 1-way ANOVA in G , I , and K .

Journal: The Journal of Clinical Investigation

Article Title: Inducible CCR2 + nonclassical monocytes mediate the regression of cancer metastasis

doi: 10.1172/JCI179527

Figure Lengend Snippet: ( A – E ) Detection of the uptake of B10F10-GFP by I-NCMs in vitro ( A – C ) and in vivo ( D and E ). Experimental design ( A ) and uptake of B16F10-GFP by RFP-labeled splenic ( B ) or blood ( C ) I-NCMs at 36 hours following coculture. The GFP signal in I-NCMs was detected by flow cytometry ( B ) or ICC ( C ). Monocytes and B16 cells were cocultured at a ratio of 5:1. White and yellow scale bars: 100 and 10 μm, respectively, in C . Experimental design ( D ) and FACS detection of uptake of B16F10-GFP materials by monocyte subsets in blood ( E , left) or lung (right) in Nr4a1 –/– mice after retro-orbital injection of MDP and B16F10-GFP injection. ( F – K ) I-NCMs recruit NK cells through CCL6 release to sites of B16F10 melanoma metastasis. ( F and G ) Adoptive transfer of I-NCMs ( F ) and MDP treatment ( G ) increased NK cells in the lungs of B16F10-bearing Nod2 –/– and Nr4a1 –/– mice, respectively. ( H ) MDP-triggered attenuation of B16F10 colonization in Nr4a1 –/– mice was inhibited by depletion of NK cells using NK1.1 antibody. ( I ) Bulk RNA-Seq data showing higher expression of Ccl6 and Ccl9 , but not other detected chemokine genes, in I-NCMs. ( J ) Anti-CCL6 antibody reduced NK cells and ( K ) suppressed the MDP-mediated attenuation of B16F10 colonization in Nr4a1 –/– mice. Data are presented as mean ± SEM; n = 4–10 in each group; * P < 0.05, ** P < 0.01, *** P < 0.001; 2-tailed t test in F and J , Kruskal-Wallis test in H , and 1-way ANOVA in G , I , and K .

Article Snippet: Anti–mouse CCL6/C10 antibody (AB-487-NA), anti-Mouse CCL9/10/MIP-1 gamma Antibody (AF463), and goat IgG isotype control (AB-108-C) were purchased from R&D Systems.

Techniques: In Vitro, In Vivo, Labeling, Flow Cytometry, Injection, Adoptive Transfer Assay, RNA Sequencing Assay, Expressing

Hog barn dust extract increases CCL9 expression in RAW264.7. Cells were treated for 1, 3, 6, or 24 h with either media or hog barn dust extract at 1% v/v and measured for CCL9. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. 1 = significant between media treatments, P < 0.05 or lower; 2 = significant between hog barn dust extract treatments, P < 0.05 or lower; 3 = significant between media and hog barn dust extract treatments, P < 0.05 or lower

Journal: Environmental disease

Article Title: Swine barn dust stimulates CCL9 expression in mouse monocytes through PKC-delta activation

doi: 10.4103/ed.ed_16_20

Figure Lengend Snippet: Hog barn dust extract increases CCL9 expression in RAW264.7. Cells were treated for 1, 3, 6, or 24 h with either media or hog barn dust extract at 1% v/v and measured for CCL9. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. 1 = significant between media treatments, P < 0.05 or lower; 2 = significant between hog barn dust extract treatments, P < 0.05 or lower; 3 = significant between media and hog barn dust extract treatments, P < 0.05 or lower

Article Snippet: The membrane was blocked with 5% milk in tris-buffered saline + 0.1% Tween20 (TBST) (0.1% Tween), followed by overnight incubation with 1:1000 dilution of rabbit anti-mouse CCL9 (500-P117, Peprotech, Rocky Hill, NJ) at 4°C.

Techniques: Expressing

CCL9 is produced in response to lipopolysaccharide and peptidoglycan. RAW264.7 cells were treated 6 h with either media, lipopolysaccharide, peptidoglycan, hog barn dust extract (1% v/v), or hog barn dust extract that was boiled for 1 h or scrubbed with polymyxin B. Bars represent CCL9 protein average of 3 replicates performed 3 times. Error bars represent standard error mean. **P < 0.01, ****P < 0.0001

Journal: Environmental disease

Article Title: Swine barn dust stimulates CCL9 expression in mouse monocytes through PKC-delta activation

doi: 10.4103/ed.ed_16_20

Figure Lengend Snippet: CCL9 is produced in response to lipopolysaccharide and peptidoglycan. RAW264.7 cells were treated 6 h with either media, lipopolysaccharide, peptidoglycan, hog barn dust extract (1% v/v), or hog barn dust extract that was boiled for 1 h or scrubbed with polymyxin B. Bars represent CCL9 protein average of 3 replicates performed 3 times. Error bars represent standard error mean. **P < 0.01, ****P < 0.0001

Techniques: Produced

Protein kinase C-δ inhibitor is involved in production of CCL9. RAW264.7 cells were treated 1 h prior to administration of hog barn dust extract with inhibitors to protein kinase C-α, δ, and ζ. hog barn dust extract was then administered and cells incubated an additional 6 h with inhibitors still present. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. *P < 0.01. NS = No significance

Journal: Environmental disease

Article Title: Swine barn dust stimulates CCL9 expression in mouse monocytes through PKC-delta activation

doi: 10.4103/ed.ed_16_20

Figure Lengend Snippet: Protein kinase C-δ inhibitor is involved in production of CCL9. RAW264.7 cells were treated 1 h prior to administration of hog barn dust extract with inhibitors to protein kinase C-α, δ, and ζ. hog barn dust extract was then administered and cells incubated an additional 6 h with inhibitors still present. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. *P < 0.01. NS = No significance

Techniques: Incubation

Protein kinase C-δ siRNA blocks CCL9 protein expression. siRNA containing either a nontargeting control (null) or protein kinase C-δ inhibiting sequence (protein kinase C -δ) was transfected into LA4 cells for 24 h prior to treatment of cells with either media or hog barn dust extract for 6 h. Release of CCL9 was measured. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. *P < 0.05, ****P < 0.0001

Journal: Environmental disease

Article Title: Swine barn dust stimulates CCL9 expression in mouse monocytes through PKC-delta activation

doi: 10.4103/ed.ed_16_20

Figure Lengend Snippet: Protein kinase C-δ siRNA blocks CCL9 protein expression. siRNA containing either a nontargeting control (null) or protein kinase C-δ inhibiting sequence (protein kinase C -δ) was transfected into LA4 cells for 24 h prior to treatment of cells with either media or hog barn dust extract for 6 h. Release of CCL9 was measured. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. *P < 0.05, ****P < 0.0001

Techniques: Expressing, Control, Sequencing, Transfection

CCL9 inhibits stimulated keratinocyte-derived chemokine protein expression. Purified CCL9 was administered (20 ng/mL) to RAW264.7 cells concurrent with lipopolysaccharide, peptidoglycan, or hog barn dust extract treatment and incubated for 6 h. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. *P < 0.05; ****P < 0.0001

Journal: Environmental disease

Article Title: Swine barn dust stimulates CCL9 expression in mouse monocytes through PKC-delta activation

doi: 10.4103/ed.ed_16_20

Figure Lengend Snippet: CCL9 inhibits stimulated keratinocyte-derived chemokine protein expression. Purified CCL9 was administered (20 ng/mL) to RAW264.7 cells concurrent with lipopolysaccharide, peptidoglycan, or hog barn dust extract treatment and incubated for 6 h. Bars represent average of 3 replicates performed 3 times. Error bars represent standard error mean. *P < 0.05; ****P < 0.0001

Techniques: Derivative Assay, Expressing, Purification, Incubation

A) Protein levels of CCL9 assessed by ELISA in paw skin in control (naive paw) (n=5), CFA + vehicle (n=9) and CFA + MCPT4 (n=5), 4 days after injections. Ordinary one-way ANOVA with multiple comparisons; p=0.0020. B) Paw withdrawal threshold of WT mice treated with CFA + vehicle or anti-CCL9 (injected 4 hours after CFA). Two-way ANOVA test with multiple comparisons; **p=0.0010; ****p<0.0001. C) Absolute number of CD11b + CD206 + cells in CFA + vehicle and CFA + anti-CCL9 treated skin (4 hours after CFA). Samples collected on day 5 post-injections. Chi-square with Fisher’s exact test. ****p<0.0001.

Journal: bioRxiv

Article Title: Mast cell-derived chymases are essential for the resolution of inflammatory pain in mice

doi: 10.1101/2024.08.05.606617

Figure Lengend Snippet: A) Protein levels of CCL9 assessed by ELISA in paw skin in control (naive paw) (n=5), CFA + vehicle (n=9) and CFA + MCPT4 (n=5), 4 days after injections. Ordinary one-way ANOVA with multiple comparisons; p=0.0020. B) Paw withdrawal threshold of WT mice treated with CFA + vehicle or anti-CCL9 (injected 4 hours after CFA). Two-way ANOVA test with multiple comparisons; **p=0.0010; ****p<0.0001. C) Absolute number of CD11b + CD206 + cells in CFA + vehicle and CFA + anti-CCL9 treated skin (4 hours after CFA). Samples collected on day 5 post-injections. Chi-square with Fisher’s exact test. ****p<0.0001.

Article Snippet: Recombinant CMA1 (Sigma-Aldrich; C8118), recombinant MCPT4 (MyBioSource; MBS1133087), or anti-CCL9 antibody (Peprotech; 500-P117) was administrated into the hind paw.

Techniques: Enzyme-linked Immunosorbent Assay, Control, Injection

Scheme 1 Schematic illustration of chemotactic C/T-NVs as a pleiotropic therapeutic strategy to eliminate metastasis SMAD4-deﬁcient colorectal cancer. (A) SMAD4-deﬁcient colorectal cancer cells ectopically express chemokine CCL9 and recruit CCR1þ-G-MDSCs to meta- static foci via the CCL9/CCR1 axis in the mouse model. CCR1þ-G-MDSCs produce excessive abundant TGF-b which directly inhibits the activity of CTLs and promotes metastasis. (B) C/T-NVs chemotactically target metastatic foci driven by the CCL9/CCR1 axis and counteract the accumulation of CCR1þ-G-MDSCs, thus suppressing CCR1þ-G-MDSCs-derived TGF-b. Tumor-inﬁltrated C/T-NVs trap excessive and essential TGF-b, thus leading to the activation of CTLs and attenuating metastasis of SMAD4-deﬁcient CRC. (C) The combination of C/T-NVs and aPD- L1 facilitates the formation of TLSs around metastatic foci, contributing to the sustained activation of CTLs and release of cytotoxic IFN-g and GzmB, and eradicates SMAD4-deﬁcient CRC.

Journal: Acta pharmaceutica Sinica. B

Article Title: CCL9/CCR1 axis-driven chemotactic nanovesicles for attenuating metastasis of SMAD4-deficient colorectal cancer by trapping TGF- β .

doi: 10.1016/j.apsb.2024.05.009

Figure Lengend Snippet: Scheme 1 Schematic illustration of chemotactic C/T-NVs as a pleiotropic therapeutic strategy to eliminate metastasis SMAD4-deﬁcient colorectal cancer. (A) SMAD4-deﬁcient colorectal cancer cells ectopically express chemokine CCL9 and recruit CCR1þ-G-MDSCs to meta- static foci via the CCL9/CCR1 axis in the mouse model. CCR1þ-G-MDSCs produce excessive abundant TGF-b which directly inhibits the activity of CTLs and promotes metastasis. (B) C/T-NVs chemotactically target metastatic foci driven by the CCL9/CCR1 axis and counteract the accumulation of CCR1þ-G-MDSCs, thus suppressing CCR1þ-G-MDSCs-derived TGF-b. Tumor-inﬁltrated C/T-NVs trap excessive and essential TGF-b, thus leading to the activation of CTLs and attenuating metastasis of SMAD4-deﬁcient CRC. (C) The combination of C/T-NVs and aPD- L1 facilitates the formation of TLSs around metastatic foci, contributing to the sustained activation of CTLs and release of cytotoxic IFN-g and GzmB, and eradicates SMAD4-deﬁcient CRC.

Article Snippet: Primary antibodies: SMAD4 (Santa Cruz, Cat# sc-7966), CCR1 (Abclonal, Cat# A18341), CCL9 (Santa Cruz, Cat# sc-74228), p-SMAD2 (Absin, Cat# abs155124) and TGF-b1 (Abclonal, Cat# A16640).

Techniques: Activity Assay, Derivative Assay, Activation Assay

Figure 1 CCR1þ-G-MDSCs accumulate to SMAD4-deﬁcient CRC tissues via the CCL15/CCR1 axis and CCL9/CCR1 axis in clinical specimens and mouse models. (A) Clinical specimens of human CRC were examined using immunohistochemistry staining for SMAD4, CCR1 and CD33, and (B) representative images of indicated specimens. Scale bar Z 100 mm. (C) Immunohistochemistry analysis of human CRC

Journal: Acta pharmaceutica Sinica. B

Article Title: CCL9/CCR1 axis-driven chemotactic nanovesicles for attenuating metastasis of SMAD4-deficient colorectal cancer by trapping TGF- β .

doi: 10.1016/j.apsb.2024.05.009

Figure Lengend Snippet: Figure 1 CCR1þ-G-MDSCs accumulate to SMAD4-deﬁcient CRC tissues via the CCL15/CCR1 axis and CCL9/CCR1 axis in clinical specimens and mouse models. (A) Clinical specimens of human CRC were examined using immunohistochemistry staining for SMAD4, CCR1 and CD33, and (B) representative images of indicated specimens. Scale bar Z 100 mm. (C) Immunohistochemistry analysis of human CRC

Techniques: Immunohistochemistry, Staining

Figure 4 C/T-NVs chemotactically target SMAD4-deﬁcient tumor cells and trap TGF-b molecules. (A) Transwell to investigate chemotactic migration of CCR1þ cells to CCL9. (B) Migratory cells on the slide were stained and photographed. CS, cultured supernatant. (C) Transwell to investigate the chemotaxis of CCR1þ NVs to SMAD4-deﬁcient cells. (D) DiO-NVs (green) and MC38 cells were stained with DAPI (blue) for CLSM image, Scale bar Z 10 mm. (E) Quantiﬁcation of the integrated density of DiO in each image analyzed by Image J, n Z 5. (F) The ex vivo biodistribution of free DiR and indicated DiR-NVs in spontaneous metastasis model at 4 and 24 h post intravenous injection. He: heart, Li: liver,

Journal: Acta pharmaceutica Sinica. B

Article Title: CCL9/CCR1 axis-driven chemotactic nanovesicles for attenuating metastasis of SMAD4-deficient colorectal cancer by trapping TGF- β .

doi: 10.1016/j.apsb.2024.05.009

Figure Lengend Snippet: Figure 4 C/T-NVs chemotactically target SMAD4-deﬁcient tumor cells and trap TGF-b molecules. (A) Transwell to investigate chemotactic migration of CCR1þ cells to CCL9. (B) Migratory cells on the slide were stained and photographed. CS, cultured supernatant. (C) Transwell to investigate the chemotaxis of CCR1þ NVs to SMAD4-deﬁcient cells. (D) DiO-NVs (green) and MC38 cells were stained with DAPI (blue) for CLSM image, Scale bar Z 10 mm. (E) Quantiﬁcation of the integrated density of DiO in each image analyzed by Image J, n Z 5. (F) The ex vivo biodistribution of free DiR and indicated DiR-NVs in spontaneous metastasis model at 4 and 24 h post intravenous injection. He: heart, Li: liver,

Techniques: Migration, Staining, Cell Culture, Chemotaxis Assay, Ex Vivo, Injection

Figure 5 C/T-NVs attenuate liver metastasis of SMAD4-deﬁcient CRC. (A) MC38-Luc cells were injected into the spleens of C57BL/6 mice. Mice received 5E11 count of indicated NVs and HBSS vehicle (i.v.), respectively. In vivo bioluminescence images of MC38-Luc metastases in indicated groups at indicated time point and (B) quantiﬁcation of liver photon ﬂux of each mouse, n Z 4. (C) MC38 cells were injected into the spleens of C57BL/6 mice. Mice received 5E11 count of indicated NVs and HBSS vehicle (i.v.), respectively. Mice were reared for 14 days and sacriﬁced for analysis of liver metastasis, n Z 4. (D) Quantiﬁcation of the liver weight, n Z 4. (E) Overall survival time of mice in indicated groups, n Z 12. (F) Quantiﬁcation of CCL9 concentration in tumors with indicated NVs treatment, n Z 3. (G) FACS analysis and quantiﬁcation of the percent of MDSCs in CD11bþ, (H) G-MDSCs in MDSCs in metastatic tumors, respectively, n Z 3. (I) Representative FACS plots of G and H. (J) Quantiﬁcation of TGF-b1 concentration in tumors with indicated NVs treatment, n Z 3. (K) FACS analysis and quantiﬁcation of the percent of CD3þ in live cells in liver metastasis, n Z 3. (L) Immunohistochemistry staining for TGF-b1 and CD3 of liver metastasis. Inset shows invasion front of liver metastasis. Scale bar Z 100 mm, scale bar for zoom out Z 30 mm. (M) FACS analysis and quantiﬁcation of the percent of CD69þ and (N) granzyme B (GzmBþ) in CD8þ cells in liver metastasis, respectively, n Z 3. Data are presented as mean SD of at least two independent experiments. Ordinary one-way ANOVA with a Tukey’s multiple comparisons test (D, F, G, H, J, K, M, N) was used for statistical analysis with calculated P values shown.

Journal: Acta pharmaceutica Sinica. B

Article Title: CCL9/CCR1 axis-driven chemotactic nanovesicles for attenuating metastasis of SMAD4-deficient colorectal cancer by trapping TGF- β .

doi: 10.1016/j.apsb.2024.05.009

Figure Lengend Snippet: Figure 5 C/T-NVs attenuate liver metastasis of SMAD4-deﬁcient CRC. (A) MC38-Luc cells were injected into the spleens of C57BL/6 mice. Mice received 5E11 count of indicated NVs and HBSS vehicle (i.v.), respectively. In vivo bioluminescence images of MC38-Luc metastases in indicated groups at indicated time point and (B) quantiﬁcation of liver photon ﬂux of each mouse, n Z 4. (C) MC38 cells were injected into the spleens of C57BL/6 mice. Mice received 5E11 count of indicated NVs and HBSS vehicle (i.v.), respectively. Mice were reared for 14 days and sacriﬁced for analysis of liver metastasis, n Z 4. (D) Quantiﬁcation of the liver weight, n Z 4. (E) Overall survival time of mice in indicated groups, n Z 12. (F) Quantiﬁcation of CCL9 concentration in tumors with indicated NVs treatment, n Z 3. (G) FACS analysis and quantiﬁcation of the percent of MDSCs in CD11bþ, (H) G-MDSCs in MDSCs in metastatic tumors, respectively, n Z 3. (I) Representative FACS plots of G and H. (J) Quantiﬁcation of TGF-b1 concentration in tumors with indicated NVs treatment, n Z 3. (K) FACS analysis and quantiﬁcation of the percent of CD3þ in live cells in liver metastasis, n Z 3. (L) Immunohistochemistry staining for TGF-b1 and CD3 of liver metastasis. Inset shows invasion front of liver metastasis. Scale bar Z 100 mm, scale bar for zoom out Z 30 mm. (M) FACS analysis and quantiﬁcation of the percent of CD69þ and (N) granzyme B (GzmBþ) in CD8þ cells in liver metastasis, respectively, n Z 3. Data are presented as mean SD of at least two independent experiments. Ordinary one-way ANOVA with a Tukey’s multiple comparisons test (D, F, G, H, J, K, M, N) was used for statistical analysis with calculated P values shown.

Techniques: Injection, In Vivo, Concentration Assay, Immunohistochemistry, Staining

Figure 4. The effects of CCL9 neutralizing antibody administered intrathecally (i.t.) according to timeline (A), at doses of 0.5, 2, and 4 µg/5 µL on mechanical (B) and thermal (C) hypersensitivity, and the inﬂuence of a CCL9 neutralizing antibody at a dose of 2 µg/5 µL plus morphine 2.5 µg/5 µL on mechanical (E) and thermal (F) hypersensitivity, administered according to timeline (D), 7 days CCI in mice. The data are presented as the mean ± SEM (naive n = 5; CCI n = 5–8). The results were evaluated using one-way ANOVA followed by Bonferroni’s post hoc test for comparisons of selected pairs. * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate signiﬁcant differences vs. V-treated group at each of the investigated time points: 1, 4, and 24 h for (B,C) graphs; * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate signiﬁcant differences vs. V + W-treated group for (E,F) graphs; # p < 0.05 indicates signiﬁcant differences between the V + M- and nAb + M-treated groups for (E,F) graphs; and & p < 0.05 indicates signiﬁcant differences between the nAb + W- and nAb + M-treated groups. Abbreviations: V: vehicle (PBS); W: vehicle (aqua pro injectione); nAb: neutralizing antibody; M: morphine; CCI: chronic constriction injury of the sciatic nerve.

Journal: Brain sciences

Article Title: Pharmacological Modulation of the MIP-1 Family and Their Receptors Reduces Neuropathic Pain Symptoms and Influences Morphine Analgesia: Evidence from a Mouse Model.

doi: 10.3390/brainsci13040579

Figure Lengend Snippet: Figure 4. The effects of CCL9 neutralizing antibody administered intrathecally (i.t.) according to timeline (A), at doses of 0.5, 2, and 4 µg/5 µL on mechanical (B) and thermal (C) hypersensitivity, and the inﬂuence of a CCL9 neutralizing antibody at a dose of 2 µg/5 µL plus morphine 2.5 µg/5 µL on mechanical (E) and thermal (F) hypersensitivity, administered according to timeline (D), 7 days CCI in mice. The data are presented as the mean ± SEM (naive n = 5; CCI n = 5–8). The results were evaluated using one-way ANOVA followed by Bonferroni’s post hoc test for comparisons of selected pairs. * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate signiﬁcant differences vs. V-treated group at each of the investigated time points: 1, 4, and 24 h for (B,C) graphs; * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate signiﬁcant differences vs. V + W-treated group for (E,F) graphs; # p < 0.05 indicates signiﬁcant differences between the V + M- and nAb + M-treated groups for (E,F) graphs; and & p < 0.05 indicates signiﬁcant differences between the nAb + W- and nAb + M-treated groups. Abbreviations: V: vehicle (PBS); W: vehicle (aqua pro injectione); nAb: neutralizing antibody; M: morphine; CCI: chronic constriction injury of the sciatic nerve.

Article Snippet: Administration of CCL3 and CCL9 Neutralizing Antibodies A single i.t. administration of CCL3 nAb (AF-450-NA, Mouse CCL3/MIP-1 alpha Antibody, R&D Systems; Minneapolis, MI, USA) or CCL9 nAb (AF463, Mouse CCL9/10/MIP-1 gamma Antibody, R&D Systems) was administered to CCI mice at the dose of 0.5, 2, or 4 μg/5 μL on Day 7, when mechanical and thermal hypersensitivity were fully developed.

Techniques:

Scheme 1. Pharmacological modulation of chemokines from MIP-1 family (CCL3 and CCL9) via neutralizing antibodies and their receptors (CCR1 by J113863, CCR5 by TAK-220 or AZD -5672) reduces neuropathic pain symptoms and inﬂuences morphine analgesia—evidence from mice model evoked by chronic constriction injury of the sciatic nerve.

Journal: Brain sciences

Article Title: Pharmacological Modulation of the MIP-1 Family and Their Receptors Reduces Neuropathic Pain Symptoms and Influences Morphine Analgesia: Evidence from a Mouse Model.

doi: 10.3390/brainsci13040579

Figure Lengend Snippet: Scheme 1. Pharmacological modulation of chemokines from MIP-1 family (CCL3 and CCL9) via neutralizing antibodies and their receptors (CCR1 by J113863, CCR5 by TAK-220 or AZD -5672) reduces neuropathic pain symptoms and inﬂuences morphine analgesia—evidence from mice model evoked by chronic constriction injury of the sciatic nerve.

Techniques:

Review

Structured Review

Images

Similar Products

Image Search Results