| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2540196 | International Immunopharmacology | 2016 | 5 Pages |
•S100G is expressed in fibroblasts following colitis induction.•The expression of S100G is down-regulated by IL-10.•S100G suppresses MCP-1 production through the inhibition of NF-κB activation.
Supplementation with interleukin (IL)-10, an important anti-inflammatory cytokine, has shown disappointing efficacy for inflammatory bowel diseases (IBD). IL-10 may down-regulate the expression of other anti-inflammatory mediators following colitis induction. We used a colitis model characterized by hapten-protein visualization, which indicates the site of hapten-protein formation after colitis induction for histological and gene expression analyses. Under IL-10 deficiency, following colitis induction inflammatory changes were reduced, and S100G expression was elevated. S100G was expressed in fibroblasts, and S100G expression was down-regulated by IL-10. S100G suppressed the production of monocyte chemotactic protein-1 (MCP-1) through the inhibition of NF-κB activation. Therefore, S100G, also known as Calbindin-D9k, may be an important anti-inflammatory mediator in fibroblasts following colitis induction, and down-regulation of S100G expression might be one reason for the insufficient performance of IL-10 supplementation.
Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slide
