IL-17A-mediated neutrophil recruitment limits expansion of segmented filamentous bacteria.

Abstract:

:Specific components of the intestinal microbiota are capable of influencing immune responses such that a mutualistic relationship is established. In mice, colonization with segmented filamentous bacteria (SFB) induces T-helper-17 (Th17) cell differentiation in the intestine, yet the effector functions of interleukin (IL)-17A in response to SFB remain incompletely understood. Here we report that colonization of mice with SFB-containing microbiota induced IL-17A- and CXCR2-dependent recruitment of neutrophils to the ileum. This response required adaptive immunity, as Rag-deficient mice colonized with SFB-containing microbiota failed to induce IL-17A, CXCL1 and CXCL2, and displayed defective neutrophil recruitment to the ileum. Interestingly, neutrophil depletion in wild-type mice resulted in significantly augmented Th17 responses and SFB expansion, which correlated with impaired expression of IL-22 and antimicrobial peptides. These data provide novel insight into a dynamic IL-17A-CXCR2-neutrophil axis during acute SFB colonization and demonstrate a central role for neutrophils in limiting SFB expansion.

journal_name

Mucosal Immunol

journal_title

Mucosal immunology

authors

Flannigan KL,Ngo VL,Geem D,Harusato A,Hirota SA,Parkos CA,Lukacs NW,Nusrat A,Gaboriau-Routhiau V,Cerf-Bensussan N,Gewirtz AT,Denning TL

doi

10.1038/mi.2016.80

subject

Has Abstract

pub_date

2017-05-01 00:00:00

pages

673-684

issue

3

eissn

1933-0219

issn

1935-3456

pii

mi201680

journal_volume

10

pub_type

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