β-Glucans in food modify colonic microflora by inducing antimicrobial protein, calprotectin, in a Dectin-1-induced-IL-17F-dependent manner

T. Kamiya, C. Tang, M. Kadoki, K. Oshima, Masahira Hattori, S. Saijo, Y. Adachi, N. Ohno, Y. Iwakura

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Dectin-1 (gene symbol: Clec7a) is a receptor for β-glucans that play an important role for the host defense against fungi. Recently, we showed that Clec7a '/' mice are resistant against dextran sodium sulfate (DSS)-induced colitis because of regulatory T-cell population expansion in the colon. The regulatory T-cell expansion is caused by expansion of commensal Lactobacillus murinus whose growth is suppressed by an antimicrobial protein, calprotectin S100A8/A9. In this report, we showed that S100A8 was mainly produced by mouse colonic epithelial cells. S100A8 was not induced directly by Dectin-1 but by Dectin-1-induced cytokines, especially interleukin-17F (IL-17F), that were produced by several types of innate immune cells including CD11c + /CD11b + myeloid cells in colonic lamina propria. S100A8/A9 heterodimer preferentially suppressed the growth of L. murinus that was increased in both Clec7a '/' and Il17f '/' mice. Furthermore, similar expansion of L. murinus and DSS-colitis resistance were observed in mice fed with β-glucan-free food. These observations suggest that food-derived β-glucans control the specific commensal microbiota via the Dectin-1-IL-17F-calprotectin axis to maintain the intestinal homeostasis.

Original languageEnglish
Pages (from-to)763-773
Number of pages11
JournalMucosal Immunology
Volume11
Issue number3
DOIs
Publication statusPublished - 2018 May 1
Externally publishedYes

Fingerprint

Leukocyte L1 Antigen Complex
Glucans
Interleukin-17
Food
Dextran Sulfate
Regulatory T-Lymphocytes
Colitis
Calgranulin A
Proteins
Microbiota
Lactobacillus
Myeloid Cells
Growth
Colon
Mucous Membrane
Homeostasis
Fungi
Epithelial Cells
Cytokines
dectin 1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

β-Glucans in food modify colonic microflora by inducing antimicrobial protein, calprotectin, in a Dectin-1-induced-IL-17F-dependent manner. / Kamiya, T.; Tang, C.; Kadoki, M.; Oshima, K.; Hattori, Masahira; Saijo, S.; Adachi, Y.; Ohno, N.; Iwakura, Y.

In: Mucosal Immunology, Vol. 11, No. 3, 01.05.2018, p. 763-773.

Research output: Contribution to journalArticle

Kamiya, T. ; Tang, C. ; Kadoki, M. ; Oshima, K. ; Hattori, Masahira ; Saijo, S. ; Adachi, Y. ; Ohno, N. ; Iwakura, Y. / β-Glucans in food modify colonic microflora by inducing antimicrobial protein, calprotectin, in a Dectin-1-induced-IL-17F-dependent manner. In: Mucosal Immunology. 2018 ; Vol. 11, No. 3. pp. 763-773.
@article{87b766d9da3f49b4932ac7adcb4e9018,
title = "β-Glucans in food modify colonic microflora by inducing antimicrobial protein, calprotectin, in a Dectin-1-induced-IL-17F-dependent manner",
abstract = "Dectin-1 (gene symbol: Clec7a) is a receptor for β-glucans that play an important role for the host defense against fungi. Recently, we showed that Clec7a '/' mice are resistant against dextran sodium sulfate (DSS)-induced colitis because of regulatory T-cell population expansion in the colon. The regulatory T-cell expansion is caused by expansion of commensal Lactobacillus murinus whose growth is suppressed by an antimicrobial protein, calprotectin S100A8/A9. In this report, we showed that S100A8 was mainly produced by mouse colonic epithelial cells. S100A8 was not induced directly by Dectin-1 but by Dectin-1-induced cytokines, especially interleukin-17F (IL-17F), that were produced by several types of innate immune cells including CD11c + /CD11b + myeloid cells in colonic lamina propria. S100A8/A9 heterodimer preferentially suppressed the growth of L. murinus that was increased in both Clec7a '/' and Il17f '/' mice. Furthermore, similar expansion of L. murinus and DSS-colitis resistance were observed in mice fed with β-glucan-free food. These observations suggest that food-derived β-glucans control the specific commensal microbiota via the Dectin-1-IL-17F-calprotectin axis to maintain the intestinal homeostasis.",
author = "T. Kamiya and C. Tang and M. Kadoki and K. Oshima and Masahira Hattori and S. Saijo and Y. Adachi and N. Ohno and Y. Iwakura",
year = "2018",
month = "5",
day = "1",
doi = "10.1038/mi.2017.86",
language = "English",
volume = "11",
pages = "763--773",
journal = "Mucosal Immunology",
issn = "1933-0219",
publisher = "Nature Publishing Group",
number = "3",

}

TY - JOUR

T1 - β-Glucans in food modify colonic microflora by inducing antimicrobial protein, calprotectin, in a Dectin-1-induced-IL-17F-dependent manner

AU - Kamiya, T.

AU - Tang, C.

AU - Kadoki, M.

AU - Oshima, K.

AU - Hattori, Masahira

AU - Saijo, S.

AU - Adachi, Y.

AU - Ohno, N.

AU - Iwakura, Y.

PY - 2018/5/1

Y1 - 2018/5/1

N2 - Dectin-1 (gene symbol: Clec7a) is a receptor for β-glucans that play an important role for the host defense against fungi. Recently, we showed that Clec7a '/' mice are resistant against dextran sodium sulfate (DSS)-induced colitis because of regulatory T-cell population expansion in the colon. The regulatory T-cell expansion is caused by expansion of commensal Lactobacillus murinus whose growth is suppressed by an antimicrobial protein, calprotectin S100A8/A9. In this report, we showed that S100A8 was mainly produced by mouse colonic epithelial cells. S100A8 was not induced directly by Dectin-1 but by Dectin-1-induced cytokines, especially interleukin-17F (IL-17F), that were produced by several types of innate immune cells including CD11c + /CD11b + myeloid cells in colonic lamina propria. S100A8/A9 heterodimer preferentially suppressed the growth of L. murinus that was increased in both Clec7a '/' and Il17f '/' mice. Furthermore, similar expansion of L. murinus and DSS-colitis resistance were observed in mice fed with β-glucan-free food. These observations suggest that food-derived β-glucans control the specific commensal microbiota via the Dectin-1-IL-17F-calprotectin axis to maintain the intestinal homeostasis.

AB - Dectin-1 (gene symbol: Clec7a) is a receptor for β-glucans that play an important role for the host defense against fungi. Recently, we showed that Clec7a '/' mice are resistant against dextran sodium sulfate (DSS)-induced colitis because of regulatory T-cell population expansion in the colon. The regulatory T-cell expansion is caused by expansion of commensal Lactobacillus murinus whose growth is suppressed by an antimicrobial protein, calprotectin S100A8/A9. In this report, we showed that S100A8 was mainly produced by mouse colonic epithelial cells. S100A8 was not induced directly by Dectin-1 but by Dectin-1-induced cytokines, especially interleukin-17F (IL-17F), that were produced by several types of innate immune cells including CD11c + /CD11b + myeloid cells in colonic lamina propria. S100A8/A9 heterodimer preferentially suppressed the growth of L. murinus that was increased in both Clec7a '/' and Il17f '/' mice. Furthermore, similar expansion of L. murinus and DSS-colitis resistance were observed in mice fed with β-glucan-free food. These observations suggest that food-derived β-glucans control the specific commensal microbiota via the Dectin-1-IL-17F-calprotectin axis to maintain the intestinal homeostasis.

UR - http://www.scopus.com/inward/record.url?scp=85048013797&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85048013797&partnerID=8YFLogxK

U2 - 10.1038/mi.2017.86

DO - 10.1038/mi.2017.86

M3 - Article

VL - 11

SP - 763

EP - 773

JO - Mucosal Immunology

JF - Mucosal Immunology

SN - 1933-0219

IS - 3

ER -