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• W2805498115 abstract "Abstract Alcohol consumption is generally well tolerated by the liver but in some individuals it results in persistent inflammation and liver disease. The mechanisms that regulate alcohol-induced liver inflammation are poorly understood. The transcription factor FOXO3 has previously been shown to be involved in suppressing alcohol-induced liver injury. In this study we demonstrate that in response to alcohol, approximately 10% of mouse hepatic macrophages undergo FOXO3-dependent apoptosis. By 3 days of alcohol exposure total hepatic macrophage numbers declined by 30% but these were restored to normal after 10 days of continued exposure. Whole body or myeloid specific Foxo3 -/- mice failed to show this apoptotic response. After 10 days of alcohol exposure, Foxo3 −/− mice had an increased basal inflammatory phenotype and an increase in the proportion of pro-inflammatory CD11b + , Ly6C + infiltrating macrophages (IMs) infiltrating. This led to marked sensitivity to LPS with a 5-fold ALT elevation and liver injury after LPS challenge in Foxo3 −/− but not WT mice. Restoring the early macrophage apoptosis burst with a pulse of intravenous GdCl 3 at day 2 had no effect on the day 10 phenotype of WT mice but it corrected the hyper-inflammatory phenotype in Foxo3 −/− mice. In conclusion, FOXO3-dependent hepatic macrophage apoptosis in response to ethanol serves to promote differentiation of infiltrating macrophages thus limiting the magnitude of the inflammatory response to ethanol." @default.
• W2805498115 created "2018-06-13" @default.
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• W2805498115 date "2018-02-13" @default.
• W2805498115 modified "2023-10-09" @default.
• W2805498115 title "FOXO3-dependent apoptosis limits alcohol-induced liver inflammation by promoting infiltrating macrophage differentiation" @default.
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• W2805498115 doi "https://doi.org/10.1038/s41420-017-0020-7" @default.
• W2805498115 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5841311" @default.
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• W2805498115 hasPublicationYear "2018" @default.
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