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

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Abd Allah M.H.; Zaalouk T.K.; Abo-Sheishaa G.A.; Shalash I.R.; Bayoumy A.S.

Journal: The Egyptian journal of immunology

Publisher: NLM (Medline)

Publication Date: 1 October 2022

Volume / Issue: Volume 29 / Issue 4

Pages: 174–183

ISSN: 11104902

DOI: 10.55133/eji.290417

Scopus: View on Scopus

PubMed: 36208046

Document Type: Article

Access: All Open Access; Bronze Open Access

Authors and Affiliations

Abd Allah M.H., Department of Medical Parasitology Faculty of Medicine, Al-Azhar University, Cairo, Egypt; Zaalouk T.K., Department of Medical Parasitology Faculty of Medicine, Al-Azhar University, Cairo, Egypt; Abo-Sheishaa G.A., Department of Medical Parasitology Faculty of Medicine, Al-Azhar University, Cairo, Egypt; Shalash I.R., Department of Medical Parasitology, Theodor Bilharz Research Institute, Giza, Egypt; Bayoumy A.S., Department of Medical Parasitology Faculty of Medicine, Al-Azhar University, Cairo, Egypt

Abstract

Schistosoma mansoni liver fibrosis is a complicated multicellular process involving numerous cytokines, chemokines, and growth factors. Transforming growth factor beta 1 (TGF- 1) and interleukin (IL)-13 have been identified as critical pro-fibrotic mediators in many studies. IL-17A was linked to enhanced TGF- and IL-13-induced pathologies. This case-control study aimed to explore the effect of IL-17A on TGF- and IL-13-induced liver fibrosis during experimentally schistosomiasis mansoni infection. A total of 40 laboratory-bred female C57BL/6 mice were divided into four equal groups (G), G1 non-infected, G2 infected wild type (WT), G3 infected/anti-IL-17 monoclonal antibodies (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- , 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. There was a significantly increased serum concentration of TGF- , IL-13, and IL-17A in infected WT mice (P<0.01), but praziquantel treatment reduced cytokine levels (P<0.03). Neutralization of IL-17A activity remarkably reduced serum concentrations of TGF- and IL-13 (P <0.03) resulting in improved liver functions and reduced granuloma size. Secretion of IL- IL-6 and TNF- were markedly enhanced by infection, however, mice that received anti-mouse IL-17 mAb displayed fewer inflammatory mediators (P<0.03). In conclusion, IL-17A might contribute to the progress of liver fibrosis by enhancing the profibrotic effect of TGF- and IL-13 in mice infected with S. mansoni. Copyright© by the Egyptian Association of Immunologists.

Citation Information

Scopus Citations: 9

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