@article{oai:nagoya.repo.nii.ac.jp:00022976,
 author = {Ishiguro, Kazuhiro and Watanabe, Osamu and Nakamura, Masanao and Yamamura, Takeshi and Ando, Takafumi and Goto, Hidemi and Hirooka, Yoshiki},
 journal = {International Immunopharmacology},
 month = {Oct},
 note = {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.},
 pages = {92--96},
 title = {S100G expression and function in fibroblasts on colitis induction},
 volume = {39},
 year = {2016}
}