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. 2021 Dec 9;12:7172. doi: 10.1038/s41467-021-27385-3

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Fig. 6 — Left panel: During homeostasis, translocation of pathobionts from the gut to the liver is a rare event. Translocated E. faecalis are cleared and phagocytosed by CRIg on Kupffer cells. Right panel: Chronic alcohol consumption results in intestinal expansion of E. faecalis. These pathobionts escape the intestinal barrier and translocate to the liver. Alcohol changes hepatic macrophage composition and phenotype, and downregulates CRIg on Kupffer cells, thus contributing to reduced CRIg expression in the liver and reducing clearance of translocated E. faecalis. Hepatic and circulating E. faecalis are recognized by TLR2, a pattern recognition receptor that binds Gram-positive bacteria, resulting in hepatic inflammation and progression of alcoholic liver disease.