BCL2 regulates antibacterial autophagy in the intestinal epithelium

• 成果类型: Article
• 署名作者: Li, Yun; Bel, Shai; Benjamin, Jamaal L.; Ruhn, Kelly A.; Hassell, Brian; Behrendt, Cassie L.; Kuang, Zheng; Hooper, Lora, V
• 署名单位: Bar Ilan University; University of Texas System; University of Texas Southwestern Medical Center; Carnegie Mellon University; University of Texas System; University of Texas Southwestern Medical Center; University of Texas System; University of Texas Southwestern Medical Center; Howard Hughes Medical Institute
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-10855
• DOI: 10.1073/pnas.2410205121
• 发表日期: 2024-12-03
• 关键词: spatial segregation; beclin; immunity; cells; phosphorylation; tumorigenesis; microbiota; proteins; promotes; innate

摘要

Autophagy is a key innate immune defense mechanism in intestinal epithelial cells. Bacterial invasion of epithelial cells activates antibacterial autophagy through a process that requires the innate immune adaptor protein MYD88, yet how MYD88 signaling connects to the autophagy machinery is unknown. Here, we show that the mouse intestriggers MYD88 signaling that regulates binding of the anti- autophagy factor B cell lymcomplex and releasing BECN1 to initiate autophagy. Mice with BCL2 phosphorylation invasion of enterocytes and dissemination to extraintestinal sites. These findings reveal that BCL2 links MYD88 signaling to enterocyte autophagy initiation, providing mechanistic insight into how invading bacteria trigger autophagy in the intestinal epithelium.