肠道神经支配的伤害感受器感觉神经元通过启动包括疼痛和炎症在内的保护性反应来对有害刺激做出反应；然而，它们在肠道感染中的作用尚不清楚.这里,我们发现，伤害性感受器神经元关键地介导宿主对细菌病原体肠道沙门氏菌伤寒沙门氏菌（STm）的防御。背根神经节伤害感受器可防止STm定植，入侵,从肠道传播。伤害感受器调节回肠Peyer’spatch(PP)卵泡相关上皮(FAE)中微折叠(M)细胞的密度以限制STm侵袭的进入点。M细胞的下游，伤害感受器维持节段丝状细菌（SFB）的水平，一种位于回肠绒毛和PPFAE上的肠道微生物，可介导对STm感染的抵抗力。TRPV1+伤害感受器通过释放降钙素基因相关肽（CGRP）直接响应STm，一种调节M细胞和SFB水平以防止沙门氏菌感染的神经肽。这些发现揭示了伤害感受器神经元在感知和防御肠道病原体中的主要作用。
Gut-innervating nociceptor sensory neurons respond to noxious stimuli by initiating protective responses including pain and inflammation; however, their role in enteric infections is unclear. Here, we find that nociceptor neurons critically mediate host defense against the bacterial pathogen Salmonella enterica serovar Typhimurium (STm). Dorsal root ganglia nociceptors protect against STm colonization, invasion, and dissemination from the gut. Nociceptors regulate the density of microfold (M) cells in ileum Peyer\'s patch (PP) follicle-associated epithelia (FAE) to limit entry points for STm invasion. Downstream of M cells, nociceptors maintain levels of segmentous filamentous bacteria (SFB), a gut microbe residing on ileum villi and PP FAE that mediates resistance to STm infection. TRPV1+ nociceptors directly respond to STm by releasing calcitonin gene-related peptide (CGRP), a neuropeptide that modulates M cells and SFB levels to protect against Salmonella infection. These findings reveal a major role for nociceptor neurons in sensing and defending against enteric pathogens.
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