Evergrande Center for Immunological Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA.
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.
J Exp Med. 2021 Sep 6;218(9). doi: 10.1084/jem.20210324. Epub 2021 Jul 21.
Mucus produced by goblet cells in the gastrointestinal tract forms a biological barrier that protects the intestine from invasion by commensals and pathogens. However, the host-derived regulatory network that controls mucus secretion and thereby changes gut microbiota has not been well studied. Here, we identify that Forkhead box protein O1 (Foxo1) regulates mucus secretion by goblet cells and determines intestinal homeostasis. Loss of Foxo1 in intestinal epithelial cells (IECs) results in defects in goblet cell autophagy and mucus secretion, leading to an impaired gut microenvironment and dysbiosis. Subsequently, due to changes in microbiota and disruption in microbiome metabolites of short-chain fatty acids, Foxo1 deficiency results in altered organization of tight junction proteins and enhanced susceptibility to intestinal inflammation. Our study demonstrates that Foxo1 is crucial for IECs to establish commensalism and maintain intestinal barrier integrity by regulating goblet cell function.
杯状细胞产生的黏液在胃肠道中形成了一道生物屏障,保护肠道免受共生菌和病原体的侵袭。然而,宿主来源的调节网络控制着黏液分泌,从而改变肠道微生物群,这一网络尚未得到很好的研究。在这里,我们发现叉头框蛋白 O1(Foxo1)通过调节杯状细胞的黏液分泌来控制肠道内稳态。肠上皮细胞(IECs)中 Foxo1 的缺失会导致杯状细胞自噬和黏液分泌缺陷,从而导致肠道微环境受损和菌群失调。随后,由于微生物群的变化和微生物组代谢物短链脂肪酸的破坏,Foxo1 的缺失会导致紧密连接蛋白的组织改变,并增强对肠道炎症的易感性。我们的研究表明,Foxo1 通过调节杯状细胞的功能对于 IECs 建立共生关系和维持肠道屏障完整性至关重要。