Differential contribution of complement receptor C5aR in myeloid and non-myeloid cells in chronic ethanol-induced liver injury in mice
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- 作者：Rebecca L. McCullougha ; Megan R. McMullena ; Dola Dasa ; Sanjoy Roychowdhurya ; Michael G. Strainicb ; M. Edward Medofb ; Laura E. Nagya ; c ; nagyL3@ccf.org" class="auth_mail" title="E-mail the corresponding author
- 关键词：4-HNE ; 4-hydroxy-2-nonenal ; ALD ; alcoholic liver disease ; ALT ; alanine aminotransferase ; C5aR ; C5a Receptor ; CCl4 ; carbon tetrachloride ; CK18 ; cytokeratin18 ; CYP2E1 ; cytochrome P450 2E1 ; IL-6 ; interleukin-6 ; MCP-1 ; macrophage chemoattractant protein-1 ; mRNA ; messenger RNA ; MLKL ; mixed lineage kinase domain-like ; RIP ; receptor-interacting protein kinase ; ROS ; reactive oxygen species ; TG ; triglyceride ; TNFα ; tumor necrosis factor-α
- 刊名：Molecular Immunology
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：75
- 期：Complete
- 页码：122-132
- 全文大小：6741 K
文摘
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Chronic ethanol-induced liver injury was studied in C5aR-/-, myeloid specific C5aR-/- and non-myeloid specific C5aR-/- mice.
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Global C5aR-/- mice were protected from ethanol-induced pro-inflammatory cytokine production but still had elevated markers of liver injury.
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Non-myeloid specific C5aR-/- expressed more pro-inflammatory mediators and hepatocyte apoptosis following chronic ethanol feeding.
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C5a increased activation of cell-protective signaling pathways and protected hepatocytes from cytotoxicity induced by ethanol and TNFα.