Abstract
ObjectiveAlthough COVID-19 is a respiratory disease, all organs can be affected including the brain. To date, specific investigations of brain injury markers (BIM) and endothelial injury markers (EIM) have been limited. Additionally, a male bias in disease severity and mortality after COVID-19 is evident globally. Sex differences in the immune response to COVID-19 may mediate this disparity. We investigated BIM, EIM and inflammatory cytokine/chemokine (CC) levels after COVID-19 and in across sexes.MethodsPlasma samples from 57 subjects at < 48 h of COVID-19 hospitalization, and 20 matched controls were interrogated for the levels of six BIMs—including GFAP, S100B, Syndecan-1, UCHLI, MAP2 and NSE, two EIMs—including sICAM1 and sVCAM1. Additionally, several cytokines/chemokines were analyzed by multiplex. Statistical and bioinformatics methods were used to measure differences in the marker profiles across (a) COVID-19 vs. controls and (b) men vs. women.ResultsThree BIMs: MAP2, NSE and S100B, two EIMs: sICAM1 and sVCAM1 and seven CCs: GRO IL10, sCD40L, IP10, IL1Ra, MCP1 and TNFα were significantly (p < 0.05) elevated in the COVID-19 cohort compared to controls. Bioinformatics analysis reveal a stronger positive association between BIM/CC/EIMs in the COVID-19 cohort. Analysis across sex revealed that several BIMs and CCs including NSE, IL10, IL15 and IL8 were significantly (p < 0.05) higher in men compared to women. Men also expressed a more robust BIM/ EIM/CC association profile compared to women.ConclusionThe acute elevation of BIMs, CCs, and EIMs and the robust associations among them at COVID-19 hospitalization are suggestive of brain and endothelial injury. Higher BIM and inflammatory markers in men additionally suggest that men are more susceptible to the risk compared to women.
Highlights
Neurologic complications after COVID-19 have been reported in both the acute and chronic period [1, 2]
Three brain injury markers (BIM): Microtubule-associated protein 2 (MAP2), neuron-specific enolase (NSE) and S100B, two endothelial injury markers (EIM): Soluble intercellular adhesion molecule-1 (sICAM1) and Soluble vascular cell adhesion molecule 1 (sVCAM1) and seven cytokine/chemokine markers (CCs): GRO IL10, sCD40L, IP10, IL1Ra, MCP1 and TNFα were significantly (p < 0.05) elevated in the COVID-19 cohort compared to controls
Analysis across sex revealed that several BIMs and CCs including NSE, IL10, IL15 and IL8 were significantly (p < 0.05) higher in men compared to women
Summary
Neurologic complications after COVID-19 have been reported in both the acute and chronic period [1, 2]. Neurologic manifestations including ischemic and hemorrhagic stroke have been reported after COVID-19. Savarraj et al Journal of Neuroinflammation (2021) 18:277 including encephalopathy, pain, chronic fatigue and cognitive dysfunction have been reported demonstrating the wide impact of COVID-19 on the nervous system [3,4,5,6,7,8]. Our understanding of the effect of COVID19 on brain injury is only beginning. COVID-19 triggers multiple pathological mechanisms—including an acute inflammatory response and endotheliopathy—and the relationship of these mechanisms with brain injury is unclear
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