伤害感受器
染色体易位
医学
神经科学
肠道细菌
创伤性脑损伤
细菌
生物
内科学
伤害
精神科
基因
受体
遗传学
作者
Xinyu You,Lin Niu,Xuejiao Song,Jiafeng Fu,Yulu Miao,Fengyin Diao,Chongming Wu,Pengwei Zhuang,Yanjun Zhang
标识
DOI:10.1016/j.bbi.2024.08.041
摘要
The prevalence of bacterial infections significantly increases among patients with severe traumatic brain injury (STBI), leading to a notable rise in mortality rates. While immune dysfunctions are linked to the incidence of pneumonia, our observations indicate that endogenous pathogens manifest in the lungs post-STBI due to the migration of gut commensal bacteria. This translocation involves gut-innervating nociceptor sensory neurons, which are crucial for host defense. Following STBI, the expression of transient receptor potential vanilloid 1 (TRPV1) in dorsal root ganglion (DRG) neurons significantly decreases, despite an initial brief increase. The timing of TRPV1 defects coincides with the occurrence of pulmonary infections post-STBI. This alteration in TRPV1
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