Abstract

Intestinal Th17 cells are induced and accumulate in response to colonization with a subgroup of intestinal microbes such as segmented filamentous bacteria (SFB) and certain extracellular pathogens. Here, we show that adhesion of microbes to intestinal epithelial cells (ECs) is a critical cue for Th17 induction. Upon monocolonization of germ-free mice or rats with SFB indigenous to mice (M-SFB) or rats (R-SFB), M-SFB and R-SFB showed host-specific adhesion to small intestinal ECs, accompanied by host-specific induction of Th17 cells. Citrobacter rodentium and Escherichia coli O157 triggered similar Th17 responses, whereas adhesion-defective mutants of these microbes failed to do so. Moreover, a mixture of 20 bacterial strains, which were selected and isolated from fecal samples of a patient with ulcerative colitis on the basis of their ability to cause a robust induction of Th17 cells in the mouse colon, also exhibited EC-adhesive characteristics.

Highlights

  • The gut microbiota contributes to the constitutive development of Th17 cells in the intestinal lamina propria (LP) (Atarashi et al, 2008; Ivanov et al, 2008)

  • We show that adhesion of microbes to intestinal epithelial cells (ECs) is a critical cue for Th17 induction

  • A mixture of 20 bacterial strains, which were selected and isolated from fecal samples of a patient with ulcerative colitis on the basis of their ability to cause a robust induction of Th17 cells in the mouse colon, exhibited EC-adhesive characteristics

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Summary

Graphical Abstract

The adhesion of specific members of the gut microbiome to intestinal epithelial cells is found to be essential for the induction of Th17 cells, highlighting location as an additional layer of regulation for the adaptive immune system. Highlights d A strong correlation between epithelial adhesion and Th17 induction by SFB and EHEC.

SUMMARY
INTRODUCTION
RESULTS
C M-SFB-mono mice
DISCUSSION
EXPERIMENTAL PROCEDURES

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