title: Involvement of interleukin-17A in pancreatic damage in rat experimental acute necrotizing pancreatitis.
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.
authors.affiliation: Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yanchang Road, Shanghai, 200072, People's Republic of China.
authors.forename: Jianbo
authors.initials: J
authors.lastname: Ni
authors.forename: Guoyong
authors.initials: G
authors.lastname: Hu
authors.forename: Jie
authors.initials: J
authors.lastname: Xiong
authors.forename: Jie
authors.initials: J
authors.lastname: Shen
authors.forename: Jiaqing
authors.initials: J
authors.lastname: Shen
authors.forename: Lijuan
authors.initials: L
authors.lastname: Yang
authors.forename: Maochun
authors.initials: M
authors.lastname: Tang
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Guojian
authors.initials: G
authors.lastname: Ying
authors.forename: Ge
authors.initials: G
authors.lastname: Yu
authors.forename: Yanling
authors.initials: Y
authors.lastname: Hu
authors.forename: Miao
authors.initials: M
authors.lastname: Xing
authors.forename: Rong
authors.initials: R
authors.lastname: Wan
authors.forename: Xingpeng
authors.initials: X
authors.lastname: Wang
mesh_terms: D061354:Acinar Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D000681:Amylases / Q000097:blood / Q000378:metabolism; D000818:Animals; D054360:Chemokine CXCL1 / Q000096:biosynthesis; D054426:Chemokine CXCL2 / Q000096:biosynthesis; D054365:Chemokine CXCL5 / Q000096:biosynthesis; D007249:Inflammation; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D053583:Interleukin-1beta / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008049:Lipase / Q000097:blood / Q000378:metabolism; D008297:Male; D010179:Pancreas / Q000473:pathology*; D058954:Pancreatic Stellate Cells / Q000187:drug effects / Q000378:metabolism; D019283:Pancreatitis, Acute Necrotizing / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000494:pharmacology; D013656:Taurocholic Acid
chemical_list: D054360:Chemokine CXCL1; D054426:Chemokine CXCL2; D054365:Chemokine CXCL5; C513297:Cxcl1 protein, rat; C513296:Cxcl2 protein, rat; D020381:Interleukin-17; D053583:Interleukin-1beta; D015850:Interleukin-6; D011994:Recombinant Proteins; D013656:Taurocholic Acid; D008049:Lipase; D000681:Amylases