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

Journal article
Authors H. Nagao-Kitamoto
J. L. Leslie
S. Kitamoto
Chunsheng Jin
Kristina A Thomsson
M. G. Gillilland
P. Kuffa
Y. Goto
R. R. Jenq
C. Ishii
A. Hirayama
A. M. Seekatz
E. C. Martens
K. A. Eaton
J. Y. Kao
S. Fukuda
P. D. R. Higgins
Niclas G. Karlsson
V. B. Young
N. Kamada
Published in Nature Medicine
ISSN 1078-8956
Publication year 2020
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Language en
Keywords germ-free mice, ulcerative-colitis, il-22, colonization, resistance, cells, transplantation, fucosylation, suppressor, adhesion, Biochemistry & Molecular Biology, Cell Biology, Research & Experimental, Medicine
Subject categories Cell biology, Biochemistry and Molecular Biology


In germ-free mice colonized with human microbiota, mucosal IL-22 signaling promotes the growth of succinate-consuming commensal bacteria via host mucus glycosylation, and transplantation of these bacteria limits Clostridioides difficile infection. 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.

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