Fan Hua, Shen Ruile, Yan Junqiang, Bai Yongjie, Fu Qizhi, Shi Xiaofei, Du Ganqin, Wang Dongmei
The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, 471003, People's Republic of China.
Drug Des Devel Ther. 2024 Dec 19;18:6145-6164. doi: 10.2147/DDDT.S489454. eCollection 2024.
This review elucidates the pivotal role of pyroptosis, triggered by gut microbiota, in the development of multiple sclerosis (MS), emphasizing its significance within the gut-brain axis. Our comprehensive analysis of recent literature reveals how dysbiosis in the gut microbiota of MS patients-characterized by reduced microbial diversity and shifts in bacterial populations-profoundly impacts immune regulation and the integrity of the central nervous system (CNS). Pyroptosis, an inflammatory form of programmed cell death, significantly exacerbates MS by promoting the release of inflammatory cytokines and causing substantial damage to CNS tissues. The gut microbiota facilitates this detrimental process through metabolites such as short-chain fatty acids and neuroactive compounds, or self-structural products like lipopolysaccharides (LPS), which modulate immune responses and influence neuronal survival. This review highlights the potential of modulating gut microbiota to regulate pyroptosis, thereby suggesting that targeting this pathway could be a promising therapeutic strategy to mitigate inflammatory responses and preserve neuronal integrity in patients with MS.
本综述阐明了由肠道微生物群引发的细胞焦亡在多发性硬化症（MS）发展中的关键作用，强调了其在肠-脑轴中的重要性。我们对近期文献的综合分析揭示了MS患者肠道微生物群的生态失调——以微生物多样性降低和细菌种群变化为特征——如何深刻影响免疫调节和中枢神经系统（CNS）的完整性。细胞焦亡是一种程序性细胞死亡的炎症形式，通过促进炎症细胞因子的释放和对CNS组织造成实质性损害，显著加剧了MS。肠道微生物群通过短链脂肪酸和神经活性化合物等代谢产物，或脂多糖（LPS）等自身结构产物促进这一有害过程，这些物质调节免疫反应并影响神经元存活。本综述强调了调节肠道微生物群以调控细胞焦亡的潜力，从而表明靶向该途径可能是一种有前景的治疗策略，以减轻MS患者的炎症反应并保护神经元完整性。
