The Effect of IL-26 on TNF-α-Induced CXCL8 Responses by Colonic Epithelial Cell Lines
| Autor: | Dennis W. McGee, Brody M. Wiles, Isabelle M Weishaar, Rebecca S. Young |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Chemokine Colon MAP Kinase Signaling System medicine.medical_treatment Immunology p38 Mitogen-Activated Protein Kinases 03 medical and health sciences 0302 clinical medicine NF-KappaB Inhibitor alpha Cell Line Tumor medicine Humans Secretion Interleukin 8 Phosphorylation Receptor Cells Cultured biology Tumor Necrosis Factor-alpha Chemistry Interleukins Interleukin-8 Interleukin Epithelial Cells General Medicine IκBα 030104 developmental biology Cytokine 030220 oncology & carcinogenesis biology.protein Cancer research Tumor necrosis factor alpha HT29 Cells Interleukin-1 |
| Zdroj: | Immunological Investigations. 48:822-834 |
| ISSN: | 1532-4311 0882-0139 |
| DOI: | 10.1080/08820139.2019.1594247 |
| Popis: | Th17 cells of the intestine and colon can produce several important cytokines during mucosal inflammation. However, few studies have focused on the role of IL-26 in intestinal inflammations. Colonic epithelial cells express receptors for IL-26, and this cytokine has been shown to induce the HT-29 colonic epithelial cell line to produce the chemokine CXCL8. However, epithelial cells would function in a cytokine network environment during mucosal inflammation and any effect of IL-26 on colonic epithelial cell chemokine responses could be affected by the presence of other potent pro-inflammatory cytokines like TNF-α and IL-1. Therefore, we investigated the effect of IL-26 with TNF-α or IL-1 on colonic epithelial cell line secretion of CXCL8. IL-26 alone had no effect on HT-29 or DLD1 cell line CXCL8 secretion. Yet, IL-26 was found to significantly enhance TNF-α-induced, but not IL-1-induced, CXCL8 secretion, but only at high levels of TNF-α. Similar results were seen with DLD1 cells. IL-26 did not enhance TNF-α-induced CXCL8 mRNA levels and did not affect TNF-α-induced IκBα phosphorylation or degradation. However, signaling through ERK and p38 MAPK were determined to be involved in the enhancing effect of IL-26 on the TNF-α-induced CXCL8 secretion, perhaps through known post-translational effects. These results suggest that the role of IL-26 in intestinal inflammation may be limited to enhancing CXCL8 secretion in the presence high levels of TNF-α, such as may occur in inflammatory bowel disease. Abbreviations: DMEM, Dulbecco's Modified Eagle's Medium; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IBD, inflammatory bowel disease; IL, interleukin; ITS, insulin, transferrin, selenium; TBS, Tris buffered saline; TNF, tumor necrosis factor. |
| Databáze: | OpenAIRE |
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