Interleukin-13 is involved in the formation of liver fibrosis in Clonorchis sinensis-infected mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2016-07

AUTHORS

Yanquan Xu, Pei Liang, Meng Bian, Wenjun Chen, Xiaoyun Wang, Jinsi Lin, Mei Shang, Hongling Qu, Zhongdao Wu, Yan Huang, Xinbing Yu

ABSTRACT

Clonorchiasis is a chronic infection disease often accompanied by formation of liver fibrosis. Previous study has identified that Clonorchis sinensis (C. sinensis, Cs) infection and CsRNASET2 (a member of CsESPs) immunization can drive Th2 immune response. IL-13, a multifunctional Th2 cytokine, has been widely confirmed to be profibrotic mediator. We want to determine whether IL-13 is involved in the generation of liver fibrosis during C. sinensis infection. A part of mice were infected with C. sinensis or immunized with CsRNASET2, respectively. Another part of mice were intravenously injected with rIL-13. Liver tissues of C. sinensis-infected mice were stained with hematoxylin-eosin and Masson's trichrome, respectively. The transcriptional levels of collagen-I, collagen-III, α-SMA, and TIMP-1 in the livers of infected mice and rIL-13-treated mice were measured by quantitative RT-PCR. Besides, splenocytes of C. sinensis-infected and CsRNASET2-immunized mice were isolated, respectively. The levels of IL-13 in splenocytes were detected by ELISA. Our results displayed that the livers of C. sinensis-infected mice had serious chronic inflammation and collagen deposition. The transcriptional levels of collagen-I, collagen-III, α-SMA, and TIMP-1 in the livers of C. sinensis-infected mice were obviously increased. Splenocytes from both C. sinensis-infected and CsRNASET2-immunized mice expressed high levels of IL-13. Moreover, rIL-13 treatment markedly promoted the transcriptional levels of collagen-I, collagen-III, α-SMA, and TIMP-1. These data implied that hepatic fibrosis was formed in the livers of C. sinensis-infected mice, and IL-13 induced by C. sinensis infection and CsRNASET2 immunization might favor this progression. More... »

PAGES

2653-2660

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00436-016-5012-7

DOI

http://dx.doi.org/10.1007/s00436-016-5012-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047083563

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26993324


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