Th17 cell induction by adhesion of microbes to intestinal epithelial cells
Open accessAbstract
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.
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Th17 cells play an important role in tissue homeostasis, especially in the intestinal mucosa.
“Th17 cells have been found to play an important role in tissue homeostasis, especially in the intestinal mucosa.”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [48]
The ability of other TH17-inducing gut bacteria to produce ATP has not been determined, but a common property appears to be their ability to adhere to the intestinal epithelium.
“The capability of other TH17-inducing gut bacteria to produce ATP has not been determined yet, but a common property appears to be their ability to adhere to the intestinal epithelium (Atarashi et al., 2015; Tan et al., 2016).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Atarashi et al., 2015
Induction of Th17 cells by SFB is enabled by their adhesion to epithelial cells.
“Induction of Th17 cells by SFB is enabled by their adhesion to epithelial cells.36”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [36]
Microbiota is involved in Th17 differentiation in the intestine and the skin, while oral barrier Th17 cell development seems to be largely independent from microbial colonization.
“While it is well established that microbiota is involved in Th17 differentiation in the intestine36 and the skin111, oral barrier Th17 cell development seems to be largely independent from microbial colonization.112”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [36]
Physical interactions between SFB and enterocytes are required for induction of Th17-polarizing molecules SAA and IL-1β.
“Physical interactions between SFB and enterocytes, to which the bacteria are tightly anchored, are required for the induction of Th17-polarizing molecules (SAA, IL-1β) [33, 34].”
From Antibiotic-Induced Changes in the Intestinal Microbiota and Disease (2016) · cites this paper as [34]
Production of antimicrobial peptides is stimulated by T helper 17 cells, which were shown to be induced by specific microbial species.
“The production of these antimicrobial peptides is stimulated by T helper 17 (TH17) cells162, which, in turn, were shown to be induced by specific microbial species163.”
From The microbiota of the respiratory tract: gatekeeper to respiratory health (2017) · cites this paper as [163]
Clostridiales are emerging as major microbial regulators of gut-derived T-cell immune and serotonergic signals that may be associated with ASD.
“the Clostridiales are emerging as major microbial regulators of gut-derived T-cell immune and serotonergic signals that may be associated with ASD.30, 31, 32, 33, 35”
From Distinct Microbiome-Neuroimmune Signatures Correlate With Functional Abdominal Pain in Children With Autism Spectrum Disorder (2017) · cites this paper as [32]
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- Authors
- Atarashi, K., Tanoue, T., Ando, M., Kamada, N., Nagano, Y., Narushima, S., Suda, W., Imaoka, A., Setoyama, H., Nagamori, T., Ishikawa, E., Shima, T., Hara, T., Kado, S., Jinnohara, T., Ohno, H., Kondo, T., Toyooka, K., Watanabe, E., Yokoyama, S.-I., Tokoro, S., Mori, H., Noguchi, Y., Morita, H., Ivanov, I. I., Sugiyama, T., Nuñez, G., Camp, J. G., Hattori, M., Umesaki, Y., & Honda, K.
- Affiliations
- Keio University (JP)
- RIKEN Center for Integrative Medical Sciences (JP)
- Yakult Central Institute (JP)
- University of Michigan (US)
- RIKEN Center for Sustainable Resource Science (JP)
- Gifu Pharmaceutical University (JP)
- Azabu University (JP)
- Japan Science and Technology Agency (JP)
- Columbia University Irving Medical Center (US)
- Max Planck Institute for Evolutionary Anthropology (DE)
- Corresponding author
- Umesaki, Yoshinori
- Honda, Kenya
- ORCID
- Atarashi, Koji
- Tanoue, Takeshi
- Ando, Minoru
- Kamada, Nobuhiko
- Nagano, Yuji
- Narushima, Seiko
- Suda, Wataru
- Ishikawa, Eiji
- Hara, Taeko
- Jinnohara, Toshi
- Ohno, Hiroshi
- Kondo, Takashi
- Toyooka, Kiminori
- Watanabe, Eiichiro
- Yokoyama, Shin-ichiro
- Mori, Hiroshi
- Ivanov, Ivaylo I.
- Sugiyama, Tsuyoshi
- Camp, J. Gray
- Hattori, Masahira
- Umesaki, Yoshinori
- Honda, Kenya
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 163
- Issue
- 2
- Pages
- 367-380
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4765954
- OpenAlex
- W2111731663
- Cited by
- 1,071
- References
- 37
- Citations by year
- 2026: 52 · 2025: 80 · 2024: 84 · 2023: 99 · 2022: 114 · 2021: 145 · 2020: 120 · 2019: 115 · 2018: 78 · 2017: 100 · 2016: 68 · 2015: 12 · 2012: 1
- FWCI
- 37.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Suzuken Memorial Foundation
- Uehara Memorial Foundation
- Keio University
- University of Tokyo
- Waksman Foundation of Japan
- Japan Society for the Promotion of Science (15H05657, 15K15076, 24687007)
- RIKEN
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK034933, R01DK098378)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- Th17 cells, intestinal epithelial cells, microbial adhesion, segmented filamentous bacteria, germ-free mice, Citrobacter rodentium, Escherichia coli O157, ulcerative colitis, gut microbiota
- MeSH terms
- Animals, Bacterial Adhesion, Bacterial Infections, Enterobacteriaceae Infections, Epithelial Cells, Escherichia coli Infections, Feces, Humans, Immunoglobulin A, Intestinal Mucosa, Mice, Inbred C57BL, Mice, Inbred Strains, Microscopy, Electron, Scanning, Rats, Inbred F344, Species Specificity, Escherichia coli O157, Citrobacter rodentium, Mice, Rats, Th17 Cells
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