Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
Staphylococcus Aureus Tames Nociceptive Neurons to Suppress Synovial Macrophage Responses for Sustained Infection in Septic Arthritis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Fang Xinyu, Chen Yang, Ding Haiqi, Huang Changyu, Hu Hongxin, Zhang Chaofan, Lin Yunzhi, Wang Qijin, Hu Xueni, Lin Yiming, Chen Yongfa, Zhang Nanxin, Yuan Xuhui, Huang Ying, Li Wenbo, Niu Susheng, Lin Jianhua, Yang Bin, Yuan Tifei, Zhang Wenming
Аннотация
The interaction between the nervous system and immune system during chronic bacterial infection remains unclear. Here, it is reported that Staphylococcus aureus (S. aureus) infection induces calcitonin gene-related peptide (CGRP) secretion from intra-articular transient receptor potential cation channel subfamily V member 1 positive (TRPV1+) nociceptive nerves through its pore-forming toxin (PFT) α-hemolysin. The released CGRP then inhibits the production of chemotactic cytokines by CX3CR1+ tissue-resident synovial lining macrophages via receptor activity modifying protein 1 (RAMP1) receptors at the onset of septic arthritis. During the subsequent chronic course of infection, the continuous release of CGRP triggered by pain has a lasting effect on the antimicrobial capabilities of macrophages, thereby promoting bacterial survival and joint damage. This evidence suggests a critical role for neuroimmune regulation in S. aureus-induced chronic septic arthritis. CGRP receptor antagonism may reduce joint destruction, thus providing a new option for treating bone and joint infections.