| Literature DB >> 28751470 |
Shai Bel1, Mihir Pendse1, Yuhao Wang1, Yun Li1, Kelly A Ruhn1, Brian Hassell1, Tess Leal1, Sebastian E Winter2, Ramnik J Xavier3,4,5, Lora V Hooper6,7.
Abstract
Intestinal Paneth cells limit bacterial invasion by secreting antimicrobial proteins, including lysozyme. However, invasive pathogens can disrupt the Golgi apparatus, interfering with secretion and compromising intestinal antimicrobial defense. Here we show that during bacterial infection, lysozyme is rerouted via secretory autophagy, an autophagy-based alternative secretion pathway. Secretory autophagy was triggered in Paneth cells by bacteria-induced endoplasmic reticulum (ER) stress, required extrinsic signals from innate lymphoid cells, and limited bacterial dissemination. Secretory autophagy was disrupted in Paneth cells of mice harboring a mutation in autophagy gene Atg16L1 that confers increased risk for Crohn's disease in humans. Our findings identify a role for secretory autophagy in intestinal defense and suggest why Crohn's disease is associated with genetic mutations that affect both the ER stress response and autophagy.Entities:
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Year: 2017 PMID: 28751470 PMCID: PMC5702267 DOI: 10.1126/science.aal4677
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728