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Hepatic macrophage iron aggravates experimental alcoholic steatohepatitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Xiong, Shigang She, Hongyun Zhang, An-Sheng Wang, Jiaohong Mkrtchyan, Hasmik Dynnyk, Alla Gordeuk, Victor R. French, Samuel W. Enns, Caroline A. Tsukamoto, Hidekazu
Description	Country affiliation: United States Author Affiliation: Xiong S ( Department of Pathology, Keck School of Medicine, University of Southern California, 1333 San Pablo St., MMR 402, Los Angeles, CA 90033-9141, USA.)
Abstract	One prime feature of alcoholic liver disease (ALD) is iron accumulation in hepatic macrophages/Kupffer cells (KC) associated with enhanced NF-kappaB activation. Our recent work demonstrates a peroxynitrite-mediated transient rise in intracellular labile iron (ILI) as novel signaling for endotoxin-induced IKK and NF-kappaB activation in rodent KC. The present study investigated the mechanism of KC iron accumulation and its effects on ILI response in experimental ALD. We also tested ILI response in human blood monocytes. Chronic alcohol feeding in rats results in increased expression of transferrin (Tf) receptor-1 and hemochromatosis gene (HFE), enhanced iron uptake, an increase in nonheme iron content, and accentuated ILI response for NF-kappaB activation in KC. Ex vivo treatment of these KC with an iron chelator abrogates the increment of iron content, ILI response, and NF-kappaB activation. The ILI response is evident in macrophages derived from human blood monocytes by PMA treatment but not in vehicle-treated monocytes, and this differentiation-associated phenomenon is essential for maximal TNF-alpha release. PMA-induced macrophages load iron dextran and enhance ILI response and TNF-alpha release. These effects are reproduced in KC selectively loaded in vivo with iron dextran in mice and more importantly aggravate experimental ALD. Our results suggest enhanced iron uptake as a mechanism of KC iron loading in ALD and demonstrate the ILI response as a function acquired by differentiated macrophages in humans and as a priming mechanism for ALD.
File Format	HTM / HTML
ISSN	01931857
e-ISSN	15221547
DOI	10.1152/ajpgi.90327.2008
Journal	AJP: Gastrointestinal and Liver Physiology
Issue Number	3
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Gastroenterology Fatty Liver, Alcoholic Metabolism Kupffer Cells Liver Animals Cation Transport Proteins Cell Differentiation Cells, Cultured Disease Models, Animal Ethanol Etiology Pathology Histocompatibility Antigens Class I Iron Chelating Agents Pharmacology Iron-dextran Complex Drug Effects Membrane Proteins Mice Mice, Inbred C57bl Nf-kappa B Rats, Wistar Receptors, Transferrin Signal Transduction Time Factors Tumor Necrosis Factor-alpha Research Support, N.i.h., Extramural Research Support, U.s. Gov't, Non-p.h.s.
Content Type	Text
Resource Type	Article
Subject	Hepatology Physiology Physiology (medical) Gastroenterology

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