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Cell Host Microbe. 2018 Mar 14;23(3):302-311.e3. doi: 10.1016/j.chom.2018.01.005. Epub 2018 Feb 22.

Commensal Microbes Induce Serum IgA Responses that Protect against Polymicrobial Sepsis.

Author information

1
Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, 36th and Hamilton Walk, 230 John Morgan Building, Philadelphia, PA 19104-6082, USA.
2
Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA.
3
Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, 36th and Hamilton Walk, 230 John Morgan Building, Philadelphia, PA 19104-6082, USA. Electronic address: dallman@pennmedicine.upenn.edu.

Abstract

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.

KEYWORDS:

B cell; IgA; antibodies; microbiota; plasma cell; sepsis; serum

PMID:
29478774
PMCID:
PMC6350773
DOI:
10.1016/j.chom.2018.01.005
[Indexed for MEDLINE]
Free PMC Article

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