Interleukin-4 retards liver fibrosis in BALB/c mice model of carbon tetra-chloride (CCl4)-associated with decreased CD80 and interleukin-12 expressions
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Background: BALB/c mice showed easily induced Th2-type responses in several infection models. Certain macrophage phenotypes contribute to liver fibrosis Aim: We characterized changes in macrophages phenotype (M1/M2) during fibrogenesis in liver fibrosis mice model.Methods: Carbon-tetrachloride (CCl4) hepatic-fibrosis was induced in BALB/c mice. Liver macrophages isolated were identified for M1 and M2 by CD80/iNOS and CD273 (programmed death ligand 2 (PDL2)/CD206, respectively. IL-4 were induced i.p along week-2 to week-4 of CCl4. Liver proteins were assessed for aSMA expressions, histology and ALT levels. Results: CCl4-induced hepatic-fibrosis showed increased CD273 (from 20.1%± 3.1in naïve mice to 27.8%±3.2 in fibrotic mice; P=0.01) while gradual decrease in CD80 (from 12%±6.2 in naïve mice to 1.97%±0.4 in fibrotic mice; P<0.02). The overall data showed decreased M1/M2 ratio. M2-macrophages showed inhibited expressions of IFN-g, IL-12 and vitamin-D-receptor (VDR) while high TGF-b levels. ALT, H&E staining intensities and SMA showed gradually increased along fibrosis while metabolic markers of serum insulin, vitamin D and VDR decreased. IL-4 inductions while inhibited fibrosis it elevated metabolic markers.Conclusion: M2-macrophages express less IFN-g and IL-12, which might indicate inability differentiation of naive T cells into Th1 cells. IL-4 has an anti-fibrotic effect through antagonize M2-macrophages of TGF-b and ameliorating insulin, vitamin D, VDR and consequently attenuated liver-fibrosis.

Journal
Title
Gastroenterology Medicine & Research
Publisher
Crimson Publishers
Publisher Country
United States of America
Indexing
Scopus
Impact Factor
None
Publication Type
Prtinted only
Volume
3
Year
2019
Pages
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