Commensal Microbes Induce Serum IgA Responses that Protect against Polymicrobial Sepsis

Publication date: Available online 22 February 2018
Source:Cell Host & Microbe
Author(s): Joel R. Wilmore, Brian T. Gaudette, Daniela Gomez Atria, Tina Hashemi, Derek D. Jones, Christopher A. Gardner, Stephen D. Cole, Ana M. Misic, Daniel P. Beiting, David Allman
Serum immunoglobulin A (IgA) antibodies are readily detected in mice and people, but the mechanisms underlying the induction of serum IgA and its role in host protection remain uncertain. We report that select commensal bacteria induce several facets of systemic IgA-mediated immunity. Exposing conventional mice to a unique but natural microflora that included several members of the Proteobacteria phylum led to T cell-dependent increases in serum IgA levels and the induction of large numbers of IgA-secreting plasma cells in the bone marrow. The resulting serum IgA bound to a restricted collection of bacterial taxa, and antigen-specific serum IgA antibodies were readily induced after intestinal colonization with the commensal bacterium Helicobacter muridarum. Finally, movement to a Proteobacteria-rich microbiota led to serum IgA-mediated resistance to polymicrobial sepsis. We conclude that commensal microbes overtly influence the serum IgA repertoire, resulting in constitutive protection against bacterial sepsis.

Graphical abstract

Teaser

Wilmore et al. demonstrate a role for serum IgA in protection against polymicrobial sepsis. Induction of protective concentrations of T cell-dependent serum IgA requires colonization of the gut with a complex microbiota that includes bacteria in the phylum Proteobacteria.


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