The influence of commensal bacteria-derived signals on basophil-associated allergic inflammation

 Abstract

Commensal bacteria that colonize mammalian mucosal surfaces are reported to influence T helper type 2 (TH2) cytokine-dependent inflammation and susceptibility to allergic disease. However, the mechanisms that underlie these observations are only beginning to be understood. We recently utilized studies of murine model systems and atopic patient populations to elucidate a mechanism by which commensal bacteria-derived signals limit serum immunoglobulin E levels, influence basophil development and steady-state circulating basophil populations and regulate basophil-associated TH2 cell responses and allergic inflammation. In this addendum, we summarize the findings of our recent work and other developments in the field, discuss the broader implications of these findings and generate new hypotheses regarding our understanding of host-commensal relationships. These areas of investigation may be applicable to the development of new preventative or therapeutic approaches to reduce the burden of allergic disease.

 Article Addendum to:

DA Hill, MC Siracusa, MC Abt, BS Kim, D Kobuley, M Kubo, T Kambayashi, DF Larosa, ED Renner, JS Orange, FD Bushman, D Artis. Commensal bacteria-derived signals regulate basophil hematopoiesis and allergic inflammation. Nat Med 2012; 18: 538- 46.
PMID: 22447074 DOI: 10.1038/nm.2657

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Pages
76 - 83
doi
10.4161/gmic.22759
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Article Addendum
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The influence of commensal bacteria-derived signals on basophil-associated allergic inflammation