tetano
Editor, Senior Moderator
Cell Mol Neurobiol
. 2023 Dec 15;44(1):2.
doi: 10.1007/s10571-023-01444-3. Microglial Inflammatory Responses to SARS-CoV-2 Infection: A Comprehensive Review
Rajen Dey[SUP] 1 [/SUP], Biswadev Bishayi[SUP] 2 [/SUP]
Affiliations
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[SUP]+[/SUP] 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.
Keywords: CCL11; COVID-19; Cytokine; Microglia; Neuroinflammation; SARS‐CoV‐2.
. 2023 Dec 15;44(1):2.
doi: 10.1007/s10571-023-01444-3. Microglial Inflammatory Responses to SARS-CoV-2 Infection: A Comprehensive Review
Rajen Dey[SUP] 1 [/SUP], Biswadev Bishayi[SUP] 2 [/SUP]
Affiliations
- PMID: 38099973
- DOI: 10.1007/s10571-023-01444-3
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[SUP]+[/SUP] 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.
Keywords: CCL11; COVID-19; Cytokine; Microglia; Neuroinflammation; SARS‐CoV‐2.