兴奋性突触后电位
运动性
生物
平衡
卡哈尔间质细胞
细胞生物学
胆碱乙酰转移酶
基因剔除小鼠
蠕动
抑制性突触后电位
神经科学
解剖
免疫学
生物化学
受体
胆碱能的
免疫组织化学
作者
Yuan Gao,Yi Shi,Mu-Xin Wei,Xiaorong Yang,Hao Yang,Haifeng Liu,Yuan Zhang,Lu Zhou,Gang Hu,Rongcun Yang
出处
期刊:Research Square - Research Square
日期:2023-06-06
标识
DOI:10.21203/rs.3.rs-2850553/v1
摘要
Abstract Peristaltic movements in gut are essential to propel ingested materials through the gastrointestinal tract. Intestinal resident macrophages play an important role in this physiological function through protecting enteric neurons. However, it is incompletely clear how individuals maintain the homeostasis of gut motility. Here we found that NLRP3 is a critical factor in controlling loss of muscularis macrophages (MMs), and demonstrate that MMs are involved in the homeostasis of excitatory neurons such as choline acetyltransferase (ChAT) + and vesicular glutamate transporter 2 (VGLUT2) + but not inhibitory neuronal nitric oxide synthase (nNOS) + neurons. NLRP3 knockout (KO) mice had enhanced gut motility and increased neurons, especially excitatory ChAT + and VGLUT2 + neurons. Single cell analyses showed that there had increased resident macrophages, especially MMs in NLRP3 KO mice. The MM proportion in the resident macrophages was markedly higher than those in wild-type (WT) or caspase 1/11 KO mice. Deletion of the MMs and transplantation of the NLRP3 KO bone marrow cells showed that survival of the gut excitatory ChAT + and VGLUT2 + neurons was dependent on the MMs. Gut microbiota metabolites β-hydroxybutyrate (BHB) could promote gut motility through protecting MMs from pyroptosis. Thus, our data suggest that MMs controlled by NLRP3 maintain the homeostasis of excitatory neurons.
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