biostudies-literatureLee CSNICHD NIH HHSNIAID NIH HHSNIMH NIH HHSNHLBI NIH HHSNIGMS NIH HHS807-20https://www.ebi.ac.uk/biostudies/studies/S-EPMC4838559biostudies-literatureUnknown44(4)Few apoptotic corpses are seen even in tissues with high cellular turnover, leading to the notion that the capacity for engulfment in vivo is vast. Whether corpse clearance can be enhanced in vivo for potential benefit is not known. In a colonic inflammation model, we noted that the expression of the phagocytic receptor Bai1 was progressively downmodulated. Consistent with this, BAI1-deficient mice had more pronounced colitis and lower survival, with many uncleared apoptotic corpses and inflammatory cytokines within the colonic epithelium. When we engineered and tested transgenic mice overexpressing BAI1, these had fewer apoptotic cells, reduced inflammation, and attenuated disease. Boosting BAI1-mediated uptake by intestinal epithelial cells (rather than myeloid cells) was important in atImmunityBoosting Apoptotic Cell Clearance by Colonic Epithelial Cells Attenuates Inflammation In Vivo.PMC4838559R01 GM107848HD074981GM064709T32 AI007496R01 GM064709F30 HL126385R01 HD074981T32-AI1007496MH096484R01 MH096484Lysiak JJRavichandran KSWheeler KMVandenabeele PLee CSJuncadella IJPenberthy KKfalseBoosting Apoptotic Cell Clearance by Colonic Epithelial Cells Attenuates Inflammation In Vivo.Few apoptotic corpses are seen even in tissues with high cellular turnover, leading to the notion that the capacity for engulfment in vivo is vast. Whether corpse clearance can be enhanced in vivo for potential benefit is not known. In a colonic inflammation model, we noted that the expression of the phagocytic receptor Bai1 was progressively downmodulated. Consistent with this, BAI1-deficient mice had more pronounced colitis and lower survival, with many uncleared apoptotic corpses and inflammatory cytokines within the colonic epithelium. When we engineered and tested transgenic mice overexpressing BAI1, these had fewer apoptotic cells, reduced inflammation, and attenuated disease. Boosting BAI1-mediated uptake by intestinal epithelial cells (rather than myeloid cells) was important in at2016-01-01T00:00:00Z2016 Apr2026-05-05T08:29:50.367Z2019-03-27T02:12:04ZS-EPMC48385592703719010.1016/j.immuni.2016.02.005