Altered regulation of Toll-like receptor responses impairs antibacterial immunity in the allergic lung.
Altered regulation of Toll-like receptor responses impairs antibacterial immunity in the allergic lung.
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肺内有细菌定植，其中一些与哮喘加重有关。使用鼻内屋尘螨致敏的过敏性气道疾病小鼠模型，我们发现新型抗菌途径不平衡，最终导致空气中中性粒细胞募集减少，并导致细菌入侵和传播。放大Toll样受体（TLR）信号传导的TREM（髓样细胞上表达的触发受体）-1和抑制该过程的TREM-2的表达被逆转。此外，内源性TLR抑制剂（A20、Tollip、SOCS 1和IRAK-M）和参与受体再循环的蛋白质（TRIAD 3）被提出。因此，中性粒细胞化学引诱物的产生减少。鼻内给予任何一种趋化因子都可以恢复招募中性粒细胞的能力，从而防止细菌入侵。因此，过敏性气道疾病的背景通过改变适合于治疗干预的关键抗菌先天免疫途径来加剧细菌感染。
The lung is colonized by commensal bacteria, some of which are associated with asthma exacerbations. Using the intranasal house-dust mite–sensitized mouse model of allergic airway disease, we show an imbalance in novel antibacterial pathways that culminates in a reduction in neutrophil recruitment to the airspaces and leads to bacterial invasion and dissemination. The expression of TREM (Triggering Receptor Expressed on Myeloid cells)-1 that amplifies Toll-like receptor (TLR) signaling and TREM-2 that inhibits this process is reversed. Furthermore, endogenous TLR inhibitors (A20, Tollip, SOCS1, and IRAK-M) and proteins involved in receptor recycling (TRIAD3) are raised. Consequently, the production of neutrophil chemoattractants is reduced. Intranasal administration of either chemokine restores the ability to recruit neutrophils, which prevents bacterial invasion. A background of allergic airway disease therefore exacerbates bacterial infection by altering key antibacterial innate immune pathways that are amenable to therapeutic intervention.
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