Microglial Inflammatory Responses to SARS‐CoV‐2 Infection: A Comprehensive Review

IF 3.6 4区 医学 Q3 CELL BIOLOGY Cellular and Molecular Neurobiology Pub Date : 2023-12-15 DOI:10.1007/s10571-023-01444-3
Rajen Dey, Biswadev Bishayi
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Abstract

Coronavirus disease 2019 (COVID-19) is primarily a respiratory disease causing a worldwide pandemic in the year of 2019. SARS‐CoV‐2 is an enveloped, positive-stranded RNA virus that could invade the host through spike protein and exhibits multi-organ effects. The Brain was considered to be a potential target for SARS‐CoV‐2 infection. Although neuropsychiatric symptoms and cognitive impairments were observed in COVID-19 patients even after recovery the mechanism of action is not well documented. In this review, the contribution of microglia in response to SARS‐CoV‐2 infection was discussed aiming to design a therapeutic regimen for the management of neuroinflammation and psycho-behavioral alterations. Priming of microglia facilitates the hyper-activation state when it interacts with SARS-CoV-2 known as the ‘second hit’. Moreover, the microgliosis produces reactive free radicals and pro-inflammatory cytokines like IL-1β, IFN-γ, and IL-6 which ultimately contribute to a ‘cytokine storm’, thereby increasing the occurrence of cognitive and neurological dysfunction. It was reported that elevated CCL11 may be responsible for psychiatric disorders and ROS/RNS-induced oxidative stress could promote major depressive disorder (MDD) and phenotypic switching. Additionally, during SARS-CoV-2 infection microglia-CD8+ T cell interaction may have a significant role in neuronal cell death. This cytokine-mediated cellular cross-talking plays a crucial role in pro-inflammatory and anti-inflammatory balance within the COVID-19 patient’s brain. Therefore, all these aspects will be taken into consideration for developing novel therapeutic strategies to combat SARS-CoV-2-induced neuroinflammation.

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小胶质细胞对 SARS-CoV-2 感染的炎症反应:全面综述
2019 年冠状病毒病(COVID-19)主要是一种呼吸道疾病,会在 2019 年引起全球大流行。SARS-CoV-2 是一种有包膜的正链 RNA 病毒,可通过尖峰蛋白侵入宿主体内,并对多个器官产生影响。大脑被认为是 SARS-CoV-2 感染的潜在目标。尽管 COVID-19 患者即使在康复后也会出现神经精神症状和认知障碍,但其作用机制尚未得到充分证实。本综述讨论了小胶质细胞在应对 SARS-CoV-2 感染中的作用,旨在设计一种治疗方案来控制神经炎症和心理行为改变。当小胶质细胞与 SARS-CoV-2 相互作用时,小胶质细胞的初始化促进了其过度激活状态,这种状态被称为 "第二击"。此外,小胶质细胞增生会产生活性自由基和促炎细胞因子,如 IL-1β、IFN-γ 和 IL-6,最终导致 "细胞因子风暴",从而增加认知和神经功能障碍的发生。据报道,CCL11 的升高可能是精神障碍的原因,ROS/RNS 诱导的氧化应激可促进重度抑郁障碍(MDD)和表型转换。此外,在 SARS-CoV-2 感染期间,小胶质细胞与 CD8+ T 细胞的相互作用可能在神经细胞死亡中发挥重要作用。这种细胞因子介导的细胞交叉对话在 COVID-19 患者大脑内的促炎和抗炎平衡中起着至关重要的作用。因此,在开发新的治疗策略以对抗 SARS-CoV-2 引起的神经炎症时,将考虑到所有这些方面。
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来源期刊
CiteScore
7.70
自引率
0.00%
发文量
137
审稿时长
4-8 weeks
期刊介绍: Cellular and Molecular Neurobiology publishes original research concerned with the analysis of neuronal and brain function at the cellular and subcellular levels. The journal offers timely, peer-reviewed articles that describe anatomic, genetic, physiologic, pharmacologic, and biochemical approaches to the study of neuronal function and the analysis of elementary mechanisms. Studies are presented on isolated mammalian tissues and intact animals, with investigations aimed at the molecular mechanisms or neuronal responses at the level of single cells. Cellular and Molecular Neurobiology also presents studies of the effects of neurons on other organ systems, such as analysis of the electrical or biochemical response to neurotransmitters or neurohormones on smooth muscle or gland cells.
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