Astroglia-mediated neuroinflammation as a putative mechanism of neurological outcomes in COVID-19? Insights from a Brazilian cohort
Ethiane Segabinazi, Fernando R Tocantins, Talita Glaser, Tamires Maglio, Nathalia C Oliveira, Andrelissa Gorete Castanha, Fabiele Baldino Russo, Paulo Emílio Corrêa Leite, Anita Brito, Camila Vieira Molina, Gabriela Prado Paludo, Raquel De Oliveira Souza, Simone Ravena Maia Alves, Marielton Dos Passos Cunha, Henning Ulrich, Edison Luiz Durigon, Paola Minoprio, Patricia C B Beltrão-Braga
Brain, Behavior, & Immunity - Health, doi:10.1016/j.bbih.2025.101115
NeuroCOVID-19 has emerged as a significant global health concern, presenting a wide spectrum of neurological manifestations, including headaches, brain fog and anosmia. While mounting evidence indicates that SARS-CoV-2 infection compromises central nervous system (CNS) function, the precise processes underlying these effects remain incompletely understood. Although neurons have been extensively studied, astrocytescritical regulators of brain homeostasis -have been largely overlooked in this context. In this study, we position astrocytes as central players in the neuropathological landscape of neuroCOVID-19, challenging their traditionally supportive role. We evaluated the frequent neurological symptoms in a Brazilian cohort of COVID-19 patients and investigated whether SARS-CoV-2 infection of cortical astrocytes induces neuroinflammation, glutamatergic imbalance, vasoregulatory disruption, and apoptosis as likely pathogenic processes. Among 162 COVID-19-positive patients, headache (53.09 %), brain fog (42.15 %), and anosmia (38.72 %) were the most commonly reported symptoms. Using human-induced pluripotent stem cell (hiPSC)-derived astrocytes, we found that SARS-CoV-2 infection promotes a pronounced pro-inflammatory response, evidenced by elevated levels of IL-6, IL-15, and IL-4 in the culture supernatant. Infected astrocytes also showed reduced mRNA expression of KLK1 and EAAT1, key genes involved in vasodilation and glutamate clearance, respectively. Additionally, a significant increase in cleaved caspase-3-positive cells indicated enhanced apoptosis. Overall, these findings demonstrate that SARS-CoV-2 disrupts astrocyte homeostatic functions, leading to neuroinflammation, excitatory neurotransmission dysregulation, and cell death that may, hypothetically, underlie the neurological sequelae of COVID-19. By reframing astrocytes as active protagonists, this study highlights their essential role in CNS vulnerability. It also suggests potential targets for the future investigation in the development of therapies against the neurological complications of COVID-19.
astrocytes and other glial populations. Such research is critical to mitigating the long-term neurological consequences of COVID-19 and reducing burden of post-COVID neurological disabilities.
CRediT authorship contribution statement Ethiane
Ethical statements The studies involving human participants were approved by the Human Research Ethics Committee of the Institute of Biomedical Sciences, of the University of São Paulo (#4.036.252). The human data presented here were obtained from the database of the project entitled "SARS-CoV-2 in the Metropolitan Region of São Paulo -Emergency Action" and the associated biorepository (#CAAE #3146620.6.0000.5467) maintained by the Institut Pasteur de São Paulo collected during the task force against COVID-19 (Cunha et al., 2021) .
Declaration of competing interest We would like to declare that Henning Ulrich has an ongoing scientific advisory role with TissueGnostics (Vienna, Austria). The other authors of "Astroglia-Mediated Neuroinflammation as a Mechanism of Neurological Outcomes in COVID-19? Insights from a Brazilian Cohort" declare no conflict interest.
Appendix A. Supplementary data Supplementary data to this article can be found online at https://doi. org/10.1016/j.bbih.2025.101115 .
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