IL-13 Signaling in Liver Fibrogenesis

Liu, Yan; Munker, Stefan; Müllenbach, Roman; Weng, Honglei

doi:10.3389/fimmu.2012.00116

Cited by 75 publications

(83 citation statements)

References 79 publications

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“…Similar to other cell types, IL-25 induced secretion of IL-13 by aPFs, but did not further their activation. IL-13 has been implicated in pathogenesis of Schistosoma mansoni infection-induced liver fibrosis (70), and recently IL-13 was shown to directly stimulate HSCs to produce CTGF and subsequently upegulate fibrogenic genes in response to nonparasite liver injury (71). Therefore, we hypothesized that following BDL, IL-25-stimulated aPFs secrete IL-13, which facilitates HSC activation (via induction of IL-13Ra2, Col1a1, Eotaxin, Tenascin-C, fibronection, and phosphorylation of ERK1/ 2).…”

Section: Ahscs and Apfs Contribute Differently To Liver Fibrosis Of Dmentioning

confidence: 99%

Origin of myofibroblasts in the fibrotic liver in mice

Iwaisako

Jiang

Zhang³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

454

461

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Significance Liver resident activated hepatic stellate cells (aHSCs), and activated portal fibroblasts (aPFs) are the major source of the fibrous scar in the liver. aPFs have been implicated in liver fibrosis caused by cholestatic liver injury, whereas fibrosis in hepatotoxic liver injury is attributed to aHSCs. However, the contribution of aPFs to cholestatic fibrosis is not well characterized because of difficulties in cell purification and the lack of identified aPF-specific markers. We have developed a novel flow cytometry-based method of aPFs purification from the nonparenchymal cell fraction of collagen-α1(I)-GFP mice and have identified potential aPF-specific markers. The goal of this study is to determine whether aPFs contribute to cholestatic liver fibrosis and identify the mechanism(s) of their activation.

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Section: Ahscs and Apfs Contribute Differently To Liver Fibrosis Of Dmentioning

confidence: 99%

Origin of myofibroblasts in the fibrotic liver in mice

Iwaisako

Jiang

Zhang³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

454

461

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“…In our research, it can be found that cori1agin extraction has an effect on granuloma formation, liver cell denaturation, inflammatory cell infiltration and connective tissue, which indicate the collagen proliferation is decreased by corilagin intervention. It has been found that IL-13, a Th2 cytokine, is a crucial pre-fibrosis factor in schistosoma egg-induced hepatic fibrosis (30,31 of responses drives the activation of hepatic stellate cells into a myofibroblast-like phenotype, and then collagen and other extracellular matrix (ECM) components are deposited (32). In this research, we found that corilagin extraction could reduce the level of IL-13 in the liver, which showed corilagin had a potential for anti-fibrosis via IL-13 signal pathway.…”

Section: Discussionmentioning

confidence: 99%

Activity of Corilagin on Post-Parasiticide Liver Fibrosis in Schistosomiasis Animal Model

Huang

Zhang

Jin

et al. 2013

Int J Immunopathol Pharmacol

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The first two authors contributed equally to this study This study investigates the effects and possible molecular mechanisms of corilagin extraction on prevention of Schistosoma japonicum ova-induced granulomas and liver fibrosis. As a result, under a light microscope, when compared to a model group, the corilagin group showed smaller granulomas, less liver cell denaturation and less inOammatory cell infiltration, and the connective tissues were significantly decreased. By Masson staining, the liver sections from the corilagin group showed less collagen distributed around granulomas, decreased liver fibrosis in the portal tracts and less formed interlobular tissue. The expression of hydroxyproline, IL-13 in liver and GATA3 in spleen in the model group was significantly higher than that in the normal group (P<0.05 or 0.01), while the level of hydroxyproline, IL-13 and GATA3 in the corilagin group were significantly lower than that in the model group (P<0.05). In conclusion, corilagin extraction can decrease the level of Th2-associated profibrotic cytokine IL-13, and down-regulate the transcription of GATA3 mRNA in spleen cells, which alleviate the hepatic fibrosis caused by egg granuloma in Schistosoma japonicum infection.Schistosomiasis is a chronic, sometimes fatal, disease with serious symptoms including liver fibrosis, ascites and splenomegaly. The main pathogen is the helminth parasite Schistosoma and the adult

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“…IL-25 binds to IL-17RA and IL-17RB heterodimers (of which IL-17RB represents an IL-25 specific moiety 85,86 ), and induces Act1-dependent activation of NFκB signaling pathway in target cells 87 . IL-25 drives the expression of IL-13 88 , which is required for suppression of Th17 responses 82–84,89,90 . We have demonstrated that IL-25 attenuates liver fibrosis in mice, suggesting that IL-25 agonists may become targets for ALD treatment 67 .…”

Section: Evidence Of the Role Of Il-17 Signaling Pathway In Aldmentioning

confidence: 99%

The Role of IL-17 Signaling in Regulation of the Liver–Brain Axis and Intestinal Permeability in Alcoholic Liver Disease

Liu

et al. 2016

Curr Pathobiol Rep

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Alcoholic liver disease (ALD) progresses from a normal liver, to steatosis, steatohepatitis, fibrosis and hepatocellular carcinoma (HCC). Despite intensive studies, the pathogenesis of ALD is poorly understood, in part due to a lack of suitable animal models which mimic the stages of ALD progression. Furthermore, the role of IL-17 in ALD has not been evaluated. We and others have recently demonstrated that IL-17 signaling plays a critical role in development of liver fibrosis and cancer. Here we summarize the most recent evidence supporting the role of IL-17 in ALD. As a result of a collaborative effort of Drs. Karin, Gao, Tsukamoto and Kisseleva, we developed several improved models of ALD in mice: 1) chronic-plus-binge model that mimics early stages of steatohepatitis, 2) intragastric ethanol feeding model that mimics alcoholic steatohepatitis and fibrosis, and 3) diethylnitrosamine (DEN)+alcohol model that mimics alcoholic liver cancer. These models might provide new insights into the mechanism of IL-17 signaling in ALD and help identify novel therapeutic targets.

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IL-13 Signaling in Liver Fibrogenesis

Cited by 75 publications

References 79 publications

Origin of myofibroblasts in the fibrotic liver in mice

Origin of myofibroblasts in the fibrotic liver in mice

Activity of Corilagin on Post-Parasiticide Liver Fibrosis in Schistosomiasis Animal Model

The Role of IL-17 Signaling in Regulation of the Liver–Brain Axis and Intestinal Permeability in Alcoholic Liver Disease

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