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

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 Th17 cell differentiation in the intestine, yet the effector functions of IL-17A i...

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Detalles Bibliográficos
Autores principales: Flannigan, Kyle L., Ngo, Vu L., Geem, Duke, Harusato, Akihito, Hirota, Simon A., Parkos, Charles A., Lukacs, Nicholas W., Nusrat, Asma, Gaboriau-Routhiau, Valérie, Cerf-Bensussan, Nadine, Gewirtz, Andrew T., Denning, Timothy L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350071/
https://www.ncbi.nlm.nih.gov/pubmed/27624780
http://dx.doi.org/10.1038/mi.2016.80
Descripción
Sumario: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 Th17 cell differentiation in the intestine, yet the effector functions of 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.