Role of IL-17A in enhancing liver fibrosis induced by TGF-β1 and IL-13 in Schistosoma mansoni infected mice

Abstract

Background: Schistosoma mansoni liver fibrosis is a complicated multicellular process involving numerous cytokines, chemokines, and growth factors. TGF-b1 and IL-13 have been identified as critical pro-fibrotic mediators in many studies. IL-17A was linked to enhanced TGF-b1 and IL-13-induced pathologies. Objective: This case-control study aimed to explore the effect of IL-17A on TGF-b1 and IL-13-induced liver fibrosis during experimentally schistosomiasis mansoni infection. Material and Methods: A total of forty laboratory-bred female C57BL/6 mice were divided into four equal groups, G1 non-infected, G2 infected wild type (WT), G3 infected/anti-IL-17 mAb and G4 treated mice. Mice were infected percutaneously with 40±5 cercariae per mouse. Neutralizing IL-17 mAb was administered to G3 intraperitoneally 3 weeks after infection and then every third day until 2 days before sacrification; mice of G4 were treated with a single dose of praziquantel. Serum levels of TGF-b1, IL-13, IL-17A and proinflammatory cytokines were measured by ELISA. Liver granulomas were identified by hematoxylin-eosin stain and measured by an ocular micrometer. Results: There was a significantly increased serum concentration of TGF-b1, IL-13, and IL-17A in infected WT mice, but praziquantel treatment reduced cytokine levels.