Department of Biochemistry, Keio University School of Medicine, Tokyo, Japan.
Japan Agency for Medical Research and Development (AMED), Core Research for Evolutional Science and Technology (CREST), Tokyo, Japan.
PLoS Biol. 2020 Sep 29;18(9):e3000813. doi: 10.1371/journal.pbio.3000813. eCollection 2020 Sep.
Short-chain fatty acids (SCFAs) produced by gastrointestinal microbiota regulate immune responses, but host molecular mechanisms remain unknown. Unbiased screening using SCFA-conjugated affinity nanobeads identified apoptosis-associated speck-like protein (ASC), an adaptor protein of inflammasome complex, as a noncanonical SCFA receptor besides GPRs. SCFAs promoted inflammasome activation in macrophages by binding to its ASC PYRIN domain. Activated inflammasome suppressed survival of Salmonella enterica serovar Typhimurium (S. Typhimurium) in macrophages by pyroptosis and facilitated neutrophil recruitment to promote bacterial elimination and thus inhibit systemic dissemination in the host. Administration of SCFAs or dietary fibers, which are fermented to SCFAs by gut bacteria, significantly prolonged the survival of S. Typhimurium-infected mice through ASC-mediated inflammasome activation. SCFAs penetrated into the inflammatory region of the infected gut mucosa to protect against infection. This study provided evidence that SCFAs suppress Salmonella infection via inflammasome activation, shedding new light on the therapeutic activity of dietary fiber.
短链脂肪酸(SCFAs)由胃肠道微生物群产生,可调节免疫反应,但宿主的分子机制尚不清楚。使用 SCFA 缀合亲和纳米珠进行的无偏筛选鉴定出凋亡相关斑点样蛋白(ASC),作为除 GPR 之外的非典型 SCFA 受体。SCFAs 通过与 ASC 的 PYRIN 结构域结合,促进巨噬细胞中的炎症小体激活。激活的炎症小体通过细胞焦亡抑制鼠伤寒沙门氏菌(S. Typhimurium)在巨噬细胞中的存活,并促进中性粒细胞募集以促进细菌清除,从而抑制宿主中的全身性传播。通过肠道细菌发酵产生 SCFA 的 SCFAs 或膳食纤维的给药通过 ASC 介导的炎症小体激活显著延长了 S. Typhimurium 感染小鼠的存活时间。SCFAs 渗透到感染的肠道黏膜的炎症区域以防止感染。这项研究提供了 SCFAs 通过炎症小体激活抑制沙门氏菌感染的证据,为膳食纤维的治疗活性提供了新的视角。