Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88

Bjørn E.V. Koch; Shuxing Yang; Gerda Lamers; Jens Stougaard; Herman P. Spaink

doi:10.1038/s41467-018-06658-4

Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88

Bjørn E.V. Koch, Shuxing Yang, Gerda Lamers, Jens Stougaard, Herman P. Spaink^*

^*Corresponding author for this work

Department of Molecular Biology and Genetics - Plant Molecular Biology

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

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Abstract

Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition.

Original language	English
Article number	4099
Journal	Nature Communications
Volume	9
Issue	1
Number of pages	11
ISSN	2041-1723
DOIs	https://doi.org/10.1038/s41467-018-06658-4
Publication status	Published - 1 Dec 2018

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title = "Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88",

abstract = "Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition.",

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Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88. / Koch, Bjørn E.V.; Yang, Shuxing; Lamers, Gerda et al.
In: Nature Communications, Vol. 9, No. 1, 4099, 01.12.2018.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

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T1 - Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88

AU - Koch, Bjørn E.V.

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AU - Spaink, Herman P.

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N2 - Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition.

AB - Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition.

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Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88

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