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Abstract
Mechanisms of bile acid–induced (BA-induced) liver injury in cholestasis are controversial, limiting development of new therapies. We examined how BAs initiate liver injury using isolated liver cells from humans and mice and in-vivo mouse models. At pathophysiologic concentrations, BAs induced proinflammatory cytokine expression in mouse and human hepatocytes, but not in nonparenchymal cells or cholangiocytes. These hepatocyte-specific cytokines stimulated neutrophil chemotaxis. Inflammatory injury was mitigated in
Authors
Shi-Ying Cai, Xinshou Ouyang, Yonglin Chen, Carol J. Soroka, Juxian Wang, Albert Mennone, Yucheng Wang, Wajahat Z. Mehal, Dhanpat Jain, James L. Boyer
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