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Neutralization of Interleukin‐17 Attenuates Cholestatic Liver Fibrosis in Mice
Author(s) -
Zhang S.,
Huang D.,
Weng J.,
Huang Y.,
Liu S.,
Zhang Q.,
Li N.,
Wen M.,
Zhu G.,
Lin F.,
Gu W.
Publication year - 2016
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12395
Subject(s) - fibrosis , liver injury , inflammation , medicine , pathogenesis , tumor necrosis factor alpha , interleukin , immunology , interleukin 17 , cd8 , liver function , pathology , cytokine , immune system
Anti‐inflammation strategy is one of the proposed therapeutic approaches to hepatic fibrosis. IL ‐17 is critical in inflammation, but the role of IL ‐17 in liver fibrosis has not yet been elucidated. In this study, we investigate the role of IL ‐17 on bile duct ligation‐induced liver injury and fibrosis in C57BL/6 mice. Animals were sacrificed at designated times, and serum and liver tissues were collected for analysis of liver function and serum IL ‐6, IL ‐1β, tumour necrosis factor‐alpha ( TNF ‐α) and transforming growth factor‐β ( TGF ‐β) levels. IL ‐17 blockade with anti‐ IL ‐17A mAb significantly improved liver function and decreased hepatocellular necrosis, pro‐inflammatory cytokines, neutrophils and macrophages influx. Furthermore, CD3 + and CD8 + lymphocytes, neutrophils and macrophages were found to express IL‐17, and neutrophils are the principal IL ‐17‐producing cells after BDL ‐induced liver injury. These data indicated that IL ‐17 signal contributes to the pathogenesis of cholestatic liver injury and blocked of IL ‐17 could potentially benefit patients with cholestatic liver disease.