Nature子刊:IL-22帮助肠道菌群抑制艰难梭菌感染
创作:szx 审核:szx 03月01日
  • 给无菌小鼠移植健康人的肠道菌群可抑制艰难梭菌感染,肠道菌群定殖诱导产生的IL-22在其中发挥关键作用;
  • IL-22信号可通过增强宿主黏液中的GlcNAc糖基化修饰,促进肠道菌群中考拉杆菌属物种的生长;
  • 考拉杆菌属物种可消耗琥珀酸盐,从而减少肠腔中可利用的琥珀酸盐(对于艰难梭菌的生长十分重要)以抑制艰难梭菌的生长;
  • 在溃疡性结肠炎患者中,MGAT4A等糖基转移酶的表达显著降低,提示IL-22介导的宿主N-糖基化修饰受损。
主编推荐语
szx
肠道菌群了介导对艰难梭菌的定殖抗性以抑制艰难梭菌感染,但宿主免疫在其中的影响尚未明确。Nature Medicine上发表的一项最新研究发现,肠道菌群定殖可诱导IL-22的产生,IL-22可增强宿主黏液的糖基化修饰,从而促进考拉杆菌属的生长,而考拉杆菌属物种可与艰难梭菌争夺琥珀酸盐以抑制后者的定殖。
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Nature Medicine [IF:36.13]

Interleukin-22-mediated host glycosylation prevents Clostridioides difficile infection by modulating the metabolic activity of the gut microbiota

IL-22介导的宿主糖基化通过调节肠道菌群的代谢活性以抑制艰难梭菌感染

10.1038/s41591-020-0764-0

02-17, Article

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Abstract:收起
The involvement of host immunity in the gut microbiota-mediated colonization resistance to Clostridioides difficile infection (CDI) is incompletely understood. Here, we show that interleukin (IL)-22, induced by colonization of the gut microbiota, is crucial for the prevention of CDI in human microbiota-associated (HMA) mice. IL-22 signaling in HMA mice regulated host glycosylation, which enabled the growth of succinate-consuming bacteria Phascolarctobacterium spp. within the gut microbiome. Phascolarctobacterium reduced the availability of luminal succinate, a crucial metabolite for the growth of C. difficile, and therefore prevented the growth of C. difficile. IL-22-mediated host N-glycosylation is likely impaired in patients with ulcerative colitis (UC) and renders UC-HMA mice more susceptible to CDI. Transplantation of healthy human-derived microbiota or Phascolarctobacterium reduced luminal succinate levels and restored colonization resistance in UC-HMA mice. IL-22-mediated host glycosylation thus fosters the growth of commensal bacteria that compete with C. difficile for the nutritional niche.

First Authors:
Hiroko Nagao-Kitamoto

Correspondence Authors:
Nobuhiko Kamada

All Authors:
Hiroko Nagao-Kitamoto,Jhansi L Leslie,Sho Kitamoto,Chunsheng Jin,Kristina A Thomsson,Merritt G Gillilland III,Peter Kuffa,Yoshiyuki Goto,Robert R Jenq,Chiharu Ishii,Akiyoshi Hirayama,Anna M Seekatz,Eric C Martens,Kathryn A Eaton,John Y Kao,Shinji Fukuda,Peter D R Higgins,Niclas G Karlsson,Vincent B Young,Nobuhiko Kamada

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