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- Title
Commensal bacteria-derived signals regulate basophil hematopoiesis and allergic inflammation.
- Authors
Hill, David A; Siracusa, Mark C; Abt, Michael C; Kim, Brian S; Kobuley, Dmytro; Kubo, Masato; Kambayashi, Taku; LaRosa, David F; Renner, Ellen D; Orange, Jordan S; Bushman, Frederic D; Artis, David
- Abstract
Commensal bacteria that colonize mammalian barrier surfaces are reported to influence T helper type 2 (TH2) cytokine-dependent inflammation and susceptibility to allergic disease, although the mechanisms that underlie these observations are poorly understood. In this report, we find that deliberate alteration of commensal bacterial populations via oral antibiotic treatment resulted in elevated serum IgE concentrations, increased steady-state circulating basophil populations and exaggerated basophil-mediated TH2 cell responses and allergic inflammation. Elevated serum IgE levels correlated with increased circulating basophil populations in mice and subjects with hyperimmunoglobulinemia E syndrome. Furthermore, B cell-intrinsic expression of myeloid differentiation factor 88 (MyD88) was required to limit serum IgE concentrations and circulating basophil populations in mice. Commensal-derived signals were found to influence basophil development by limiting proliferation of bone marrow-resident precursor populations. Collectively, these results identify a previously unrecognized pathway through which commensal-derived signals influence basophil hematopoiesis and susceptibility to TH2 cytokine-dependent inflammation and allergic disease.
- Subjects
BASOPHILS; T helper cells; IMMUNOGLOBULIN E; MYELOID differentiation factor 88; DISEASE susceptibility
- Publication
Nature Medicine, 2012, Vol 18, Issue 4, p538
- ISSN
1078-8956
- Publication type
Article
- DOI
10.1038/nm.2657