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Tissue-resident macrophages and Kupffer cells have also been shown to play a key role in the liver after acetaminophen-induced acute liver failure (AALF) in mice and humans.
During AALF, a marked increase in inflammatory macrophages is observed in areas of hepatic necrosis, whereas circulating monocytes are generally reduced (the lowest amounts are observed in patients who develop adverse outcomes; Antoniades et al.
The tissue-resident macrophages are thought to quickly convert to a pro-resolution tissue-repair phenotype during AALF, so ex- panding their numbers through local proliferation or recruitment from the monocyte pool has been hypothesized to be a critical determinant controlling survival following severe liver injury.
In support of this conclusion, recent studies of AALF and partial hepatectomy in mice have shown that by expanding the number of tissue-resident macrophages and recruited monocytes exhib- iting a reparative anti-inflammatory phenotype, colony-stimu- lating factor 1-Fc treatment holds promise as a therapeutic strat- egy after acute liver injury (Stutchfield et al.
Source and characterization of hepatic macrophages in acetaminophen-induced acute liver failure in humans.
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