| Literature DB >> 22990529 |
Jianbo Ni1, Guoyong Hu, Jie Xiong, Jie Shen, Jiaqing Shen, Lijuan Yang, Maochun Tang, Yan Zhao, Guojian Ying, Ge Yu, Yanling Hu, Miao Xing, Rong Wan, Xingpeng Wang.
Abstract
Interleukin (IL)-17A is a proinflammatory cytokine, which has recently attracted much interest due to its pathogenic role in various inflammatory conditions such as ischemia/reperfusion injury, chronic inflammation, and autoimmune diseases, but the role of IL-17A in acute pancreatitis remains unclear. This study aimed to investigate the role of IL-17A in experimental acute necrotizing pancreatitis (ANP). We analyzed the expression of IL-17A during the pathogenesis of ANP in vivo induced by 3 % sodium taurocholate (NaTc), by microarray test, quantitative real-time PCR, Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry. The effects of IL-17A on pancreatic acinar cells and pancreatic stellate cells (PSCs) were further investigated in vitro using recombinant rat IL-17A (rIL-17A). Expression of IL-17A was significantly increased following experimental acute pancreatitis. In addition, rIL-17A induced rat pancreatic acinar cell necrosis and promoted expression of several target genes, including IL-6, IL-1β, CXCL1, CXCL2, and CXCL5, in acinar cells and PSCs. These findings suggest that IL-17A may be involved in pancreatic damage by regulating the expression of inflammatory cytokines and chemokines during experimental acute pancreatitis.Entities:
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Year: 2013 PMID： 22990529 DOI： 10.1007/s10753-012-9519-5
Source DB: PubMed Journal: Inflammation ISSN： 0360-3997 Impact factor: 4.092