qiita_sid_11513
Gut microbiota utilize immunoglobulin A for mucosal colonization
While it is known that many strains of bacteria persist for years within individuals, mechanisms that govern the steady-state stability of the gut microbiome remain poorly understood. We have discovered a sensor/regulatory system in the human commensal Bacteroides fragilis that modulates remodeling of its surface architecture to invite binding of immunoglobulin A (IgA), which promotes formation of bacterial aggregates in mucus and adherence to intestinal epithelial cells. Generation of IgA that binds the surface of B. fragilis is required for bacteria to occupy a defined mucosal niche that mediates stable colonization of the gut. Therefore, in addition to its role in pathogen clearance, we found that IgA responses are co-opted by the microbiome to enable host-microbial symbiosis. We have designed a sequencing experiment to test our theory with a full mouse microbiome using gnotobiotic wildtype and IgA knockout mice.
While it is known that many strains of bacteria persist for years within individuals, mechanisms that govern the steady-state stability of the gut microbiome remain poorly understood. We have discovered a sensor/regulatory system in the human commensal Bacteroides fragilis that modulates remodeling of its surface architecture to invite binding of immunoglobulin A (IgA), which promotes formation of bacterial aggregates in mucus and adherence to intestinal epithelial cells. Generation of IgA that binds the surface of B. fragilis is required for bacteria to occupy a defined mucosal niche that mediates stable colonization of the gut. Therefore, in addition to its role in pathogen clearance, we found that IgA responses are co-opted by the microbiome to enable host-microbial symbiosis. We have designed a sequencing experiment to test our theory with a full mouse microbiome using gnotobiotic wildtype and IgA knockout mice.