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.

Details

Title
Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88
Author
Koch, Bjørn E V 1   VIAFID ORCID Logo  ; Yang, Shuxin 2 ; Lamers, Gerda 3 ; Stougaard, Jens 4   VIAFID ORCID Logo  ; Spaink, Herman P 3   VIAFID ORCID Logo 

1  Institute of Biology, Leiden University, Leiden, The Netherlands; Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark 
2  Institute of Biology, Leiden University, Leiden, The Netherlands; Center for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China 
3  Institute of Biology, Leiden University, Leiden, The Netherlands 
4  Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark 
Pages
1-11
Publication year
2018
Publication date
Oct 2018
Publisher
Nature Publishing Group
e-ISSN
20411723
Source type
Scholarly Journal
Language of publication
English
DOI
https://doi.org/10.1038/s41467-018-06658-4
ProQuest document ID
2116607182
Copyright
© 2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.