antibodies against il 8 (R&D Systems)
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antibodies against il 8
Antibodies Against Il 8, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 241 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+il+8+cxcl8+antibody/Human+IL-8%2FCXCL8+Antibody/pmc13624310-144-5-11
Average 95 stars, based on 241 article reviews
Antibodies Against Il 8, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 241 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+il+8+cxcl8+antibody/Human+IL-8%2FCXCL8+Antibody/pmc13624310-144-5-11
Average 95 stars, based on 241 article reviews
antibodies against il 8 - by Bioz Stars,
2026-10
95/100 stars
Images
1) Product Images from "MIIP Inhibits Colorectal Cancer Progression by Modulating Neutrophils Infiltration and Neutrophil Extracellular Trap Formation"
Article Title: MIIP Inhibits Colorectal Cancer Progression by Modulating Neutrophils Infiltration and Neutrophil Extracellular Trap Formation
Journal: Advanced Science
doi: 10.1002/advs.78063
Figure Legend Snippet: MIIP in CRC cells inhibits neutrophil infiltration and NETs formation through IL‐8. (A) Human cytokine array of the CM collected from SW620 cells with vector control and MIIP overexpression. (B) ELISA quantification of secreted IL‐8 protein levels in CM derived from three CRC cell lines with differential MIIP expression ( n = 3). (C) Volcano plot of DEGs from RNA‐seq analysis of CRC cell lines with varying levels of MIIP expression ( n = 3 per group). (D) CXCL8 mRNA expression in human CRC cells with different levels of MIIP expression was tested by RT–qPCR ( n = 3). (E) Quantification of neutrophils that migrated to CRC CM with or without recombinant human IL‐8 protein (rhIL‐8). Quantification of neutrophils that migrated to the CRC CM with or without anti‐IL‐8 neutralizing antibody (N‐IL‐8) ( n = 3). (F–H) Representative images and statistical quantification of IF staining ( n = 5) and MPO‐DNA ELISA ( n = 3) for NETs formation after neutrophils were co‐cultured with the CM from SW620 cells treated with recombinant IL‐8 protein and with the CM from SW480 and HCT116 cells treated with an anti‐IL‐8 neutralizing antibody. Scale bar, 50 µm. All the data are shown as the mean ± SD; * , p < 0.05; ** , p < 0.01; *** , p < 0.001. NS, not significant. Statistical significance was assessed using Student's t‐test and two‐way ANOVA in (B, D, E, G, and H).
Techniques Used: Plasmid Preparation, Control, Over Expression, Enzyme-linked Immunosorbent Assay, Derivative Assay, Expressing, RNA Sequencing, Analysis, Quantitative RT-PCR, Recombinant, Staining, Cell Culture
Figure Legend Snippet: MIIP in CRC cells decreases neutrophil infiltration and NETs formation through NF‐κB p65/IL‐8 signaling. (A) Bubble plot of the enriched KEGG pathways showing that the NF‐κB signaling pathway was enriched in HCT116 cells (marked with a red border). (B) GSEA revealed that MIIP knockdown in HCT116 cells significantly activated the NF‐κB signaling pathway. (C) Western blotting analysis of key proteins involved in the NF‐κB p65 signaling pathway in human CRC cells with different levels of MIIP expression. (D) Representative images of H&E and IHC staining for MIIP, p‐p65, IL‐8, and Ly6G in tumors from the cecum of an orthotopic CRC mouse model between the MIIP‐overexpressing group and the control group (n = 5 per group). Scale bar, 50 µm. (E) Statistical analysis of Ly6G + neutrophils and the expression of p‐p65 and IL‐8 in different groups. (F) Representative images and statistical quantification of IF staining for MPO (red), Cit‐H3 (green), and DAPI (blue) in tumor tissue from the cecum and comparisons between the two groups ( n = 5). Scale bar, 25 µm. (G) Western blotting of NF‐κB p65 and NF‐κB p‐p65 in CRC cells treated with or not treated with an NF‐κB inhibitor (Bay 11–7082, 10 µM). (H) RT‐qPCR of CXCL8 mRNA in CRC cells treated or not treated with an NF‐κB inhibitor ( n = 3). (I) ELISA of IL‐8 in CM from CRC cells treated or not treated with an NF‐κB inhibitor ( n = 3). (J) Quantification of neutrophils that migrated to the CM from CRC cells treated or not treated with an NF‐κB inhibitor ( n = 3). (K–M) ELISA of MPO‐DNA and representative images and statistical quantification of IF staining for NETs formation after neutrophils were cultured with CM from SW480 and HCT116 cells treated or not treated with an NF‐κB inhibitor ( n = 3–5). Scale bar, 50 µm. All the data are shown as the mean ± SD; * , p < 0.05; ** , p < 0.01; *** , p < 0.001. NS, not significant. Statistical significance was assessed using Student's t‐test and the Mann‐Whitney U test in (E); the Mann‐Whitney U test in (F); and two‐way ANOVA in (H, I, J, K, and M).
Techniques Used: Knockdown, Western Blot, Analysis, Expressing, Immunohistochemistry, Control, Staining, Tissue, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cell Culture, MANN-WHITNEY
Figure Legend Snippet: MIIP modulates the NF‐κB p65/IL‐8 signaling pathway ‐mediated neutrophil infiltration and NETs formation through interactions with PKR. (A) IP–MS revealed PKR as a MIIP‐interacting protein. (B) The binding structure of MIIP and PKR was predicted using HDOCK molecular docking software. (C) Endogenous interaction between MIIP and PKR were detected via Co‐IP in HCT116 cells. (D) 293T cells were cotransfected with MIIP‐Flag and PKR‐HA, and reverse and forward Co‐IP analyses were performed. (E) Co‐IP assays were used to determine the PKR‐binding region of MIIP. (F) Co‐IP assays revealed that the PKR binding site for MIIP encompasses its IKKβ‐binding domain. (G) The expression of PKR was determined by Western blotting in CRC cells with different levels of MIIP expression. (H) Co‐IP was performed to examine the effect of MIIP expression on the interaction between PKR and IKKβ. (I–M) Double‐stable transgenic CRC cell lines were used in a rescue assay to demonstrate that the regulatory effects of MIIP on the NF‐κB p65‐mediated IL‐8 signaling pathway (I–K) and NETs formation (L, M) were dependent on PKR ( n = 3–5). All the data are shown as the mean ± SD; * , p < 0.05; ** , p < 0.01; *** , p < 0.001. NS, not significant. Statistical significance was assessed using two‐way ANOVA in (J–M).
Techniques Used: Protein-Protein interactions, Binding Assay, Docking Assay, Software, Co-Immunoprecipitation Assay, Expressing, Western Blot, Transgenic Assay, Rescue Assay
Figure Legend Snippet: Schematic illustration shows that MIIP inhibits colorectal cancer progression by decreasing TANs infiltration and NETs formation through the PKR/NF‐κB p65/IL‐8 axis, providing potential therapeutic strategies for colorectal cancer.
Techniques Used:
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