Commensal bacteria-derived signals regulate basophil hematopoiesis and allergic inflammation.
Commensal bacteria-derived signals regulate basophil hematopoiesis and allergic inflammation.
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据报道，定植于哺乳动物屏障表面的共生细菌会影响 2 型辅助 T (TH2) 细胞因子依赖性炎症和过敏性疾病的易感性，尽管这些观察结果背后的机制尚不清楚。在本报告中，我们发现通过口服抗生素治疗故意改变共生细菌群体会导致血清免疫球蛋白 E (IgE) 水平升高、稳态循环嗜碱性粒细胞群体增加、以及夸大嗜碱性粒细胞介导的 TH2 细胞反应和过敏性炎症。在患有高免疫球蛋白血症 E 综合征的小鼠和受试者中，血清 IgE 水平升高与循环嗜碱性粒细胞数量增加相关。此外，B 细胞内在表达 MyD88 是限制小鼠血清 IgE 水平和循环嗜碱性粒细胞数量所必需的。研究发现共生源信号通过限制骨髓前体细胞的增殖来影响嗜碱性粒细胞的发育。总的来说，这些结果确定了一个以前未被认识的途径，共生源信号通过该途径影响嗜碱性粒细胞造血以及对 TH2 细胞因子依赖性炎症和过敏性疾病的易感性。
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 identify that deliberate alteration of commensal bacterial populations via oral antibiotic treatment resulted in elevated serum immunoglobulin E (IgE) levels, 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 MyD88 was required to limit serum IgE levels 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.
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