Duve Khrystyna, Petakh Pavlo, Kamyshnyi Oleksandr
Department of Neurology, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.
Department of Biochemistry and Pharmacology, Uzhhorod National University, Uzhhorod, Ukraine.
Front Microbiol. 2024 May 28;15:1406874. doi: 10.3389/fmicb.2024.1406874. eCollection 2024.
While neurological complications of COVID-19, such as encephalopathy, are relatively rare, their potential significant impact on long-term morbidity is substantial, especially given the large number of infected patients. Two proposed hypotheses for the pathogenesis of this condition are hypoxia and the uncontrolled release of proinflammatory cytokines. The gut microbiota plays an important role in regulating immune homeostasis and overall gut health, including its effects on brain health through various pathways collectively termed the gut-brain axis. Recent studies have shown that COVID-19 patients exhibit gut dysbiosis, but how this dysbiosis can affect inflammation in the central nervous system (CNS) remains unclear. In this context, we discuss how dysbiosis could contribute to neuroinflammation and provide recent data on the features of neuroinflammation in COVID-19 patients.
虽然新冠病毒感染的神经系统并发症,如脑病,相对罕见,但鉴于感染患者数量众多,它们对长期发病率的潜在重大影响是巨大的。关于这种病症发病机制的两个提出的假说是缺氧和促炎细胞因子的失控释放。肠道微生物群在调节免疫稳态和整体肠道健康方面发挥着重要作用,包括通过统称为肠脑轴的各种途径对大脑健康产生影响。最近的研究表明,新冠病毒感染患者存在肠道菌群失调,但这种失调如何影响中枢神经系统(CNS)的炎症仍不清楚。在此背景下,我们讨论菌群失调如何导致神经炎症,并提供新冠病毒感染患者神经炎症特征的最新数据。