Gut microbiota utilize immunoglobulin A for mucosal colonization
Author(s) -
Gregory P. Donaldson,
Mark S. Ladinsky,
Kristie B. Yu,
Jon G. Sanders,
Byouengmin Yoo,
WenChi Chou,
Margaret E. Conner,
Ashlee M. Earl,
Rob Knight,
Pamela J. Björkman,
Sarkis K. Mazmanian
Publication year - 2018
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aaq0926
Subject(s) - bacteroides fragilis , colonization , microbiome , biology , immunoglobulin a , immune system , microbiology and biotechnology , commensalism , antibody , colonisation resistance , niche , immunology , pathogen , gut flora , dysbiosis , bacteroides , immunoglobulin g , bacteria , ecology , genetics , antibiotics
The immune system responds vigorously to microbial infection while permitting lifelong colonization by the microbiome. Mechanisms that facilitate the establishment and stability of the gut microbiota remain poorly described. We found that a regulatory system in the prominent human commensal Bacteroides fragilis modulates its surface architecture to invite binding of immunoglobulin A (IgA) in mice. Specific immune recognition facilitated bacterial adherence to cultured intestinal epithelial cells and intimate association with the gut mucosal surface in vivo. The IgA response was required for B. fragilis (and other commensal species) to occupy a defined mucosal niche that mediates stable colonization of the gut through exclusion of exogenous competitors. Therefore, in addition to its role in pathogen clearance, we propose that IgA responses can be co-opted by the microbiome to engender robust host-microbial symbiosis.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom