Evaluating Microglia & Astrocyte ‘Cross-talk’ in Sustained Neuroinflammation Secondary to COVID-19 & TBI

The long-term neurological impacts of COVID-19 reflect an emerging field of research, and the need to appreciate their physiology as it relates to biochemical and molecular pathways proves understudied. Independent of one another, traumatic brain injury (TBI) and COVID-19 can lead to increased risk for neurodegenerative diseases, yet this phenomenon and their combined impacts remain largely unknown. This novel research study investigates the combined impacts of COVID-19 infection and TBI on sustained neuroinflammation, a possible mechanism for underlying and prolonged neurological symptoms. In particular, this research evaluates the extent of microglia and astrocyte “cross-talk,” given their known individual roles in neuroinflammatory processes, and their communication facilitated by exosomes. It was hypothesized that patients with a history of both COVID-19 and TBI may exhibit sustained neuroinflammation due to the combined interaction of these conditions, which reflects the combined response of microglial and astrocytic activation secondary to the neuroinflammatory responses initiated by injury and viral illness - like those of COVID-19 and TBI - transmitted through the contents of exosomes that induce a neuroinflammatory or CNS immune response.

To evaluate this, BV2 microglial cells were treated with human patient astrocyte-derived exosomes to appreciate the “cross-talk” between the microglia and astrocytes that may be facilitated by exosomes. Understanding the interplay between COVID-19 and TBI in sustaining neuroinflammation proves crucial for developing targeted therapeutic interventions. By bridging the gap between symptomatology and pathology, this research lays the foundation for potential therapeutic strategies to alleviate neurological symptoms in patients with histories of COVID-19 and TBI, addressing an emerging and pressing need in post-COVID-19 pandemic global health.