Lung-innervating nociceptor sensory neurons detect noxious or harmful stimuli and consequently protect organisms by mediating coughing, pain, and bronchoconstriction. However, the role of sensory neurons in pulmonary host defense is unclear. Here, we found that TRPV1⁺ nociceptors suppressed protective immunity against lethal Staphylococcus aureus pneumonia. Targeted TRPV1⁺-neuron ablation increased survival, cytokine induction, and lung bacterial clearance. Nociceptors suppressed the recruitment and surveillance of neutrophils, and altered lung γδ T cell numbers, which are necessary for immunity. Vagal ganglia TRPV1⁺ afferents mediated immunosuppression through release of the neuropeptide calcitonin gene-related peptide (CGRP). Targeting neuroimmunological signaling may be an effective approach to treat lung infections and bacterial pneumonia.

中文翻译：

---

伤害感受神经元抑制细菌肺部感染和致死性肺炎中的中性粒细胞和γδT细胞反应。

肺神经伤害感受器感觉神经元检测到有害或有害刺激，因此通过介导咳嗽，疼痛和支气管收缩来保护生物体。然而，尚不清楚感觉神经元在肺宿主防御中的作用。在这里，我们发现TRPV1 ⁺伤害感受器抑制了针对致死性金黄色葡萄球菌肺炎的保护性免疫。靶向TRPV1 ^+-神经元消融可提高生存率，细胞因子诱导和肺细菌清除率。伤害感受器抑制了嗜中性粒细胞的募集和监视，并改变了免疫所需的肺γδT细胞数量。迷走神经节TRPV1 ⁺通过释放神经肽降钙素基因相关肽（CGRP）介导免疫抑制。靶向神经免疫信号可能是治疗肺部感染和细菌性肺炎的有效方法。