PUBLICATION

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

Authors
Koch, B.E.V., Yang, S., Lamers, G., Stougaard, J., Spaink, H.P.
ID
ZDB-PUB-181007-3
Date
2018
Source
Nature communications   9: 4099 (Journal)
Registered Authors
Koch, Bjorn, Spaink, Herman P.
Keywords
none
Datasets
GEO:GSE82200
MeSH Terms
  • Animals
  • Gastrointestinal Microbiome/immunology*
  • Genes, Reporter
  • Immunity, Innate*
  • Intestinal Mucosa/immunology*
  • Myeloid Differentiation Factor 88/genetics
  • Myeloid Differentiation Factor 88/metabolism*
  • Toll-Like Receptor 2/metabolism
  • Transcriptome
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
30291253 Full text @ Nat. Commun.
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.
Errata / Notes
This article is corrected by ZDB-PUB-220906-137 .
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping