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Narsoplimab (anti-MASP2) modulates long COVID patient plasma-induced transcriptional responses in human microvascular endothelial cells

ABSTRACT: Fourteen percent of SARS-CoV-2-infected individuals suffer multi-organ dysfunction and are unable to resume employment for >2 years post-acute COVID-19. Such "long COVID" cases have been linked to SARS-CoV-2 reservoirs and sustained complement activation. We examined the effects of lectin complement pathway MASP2 inhibitor narsoplimab on long COVID patient plasma-driven microvascular endothelial cell (MVEC) injury, comparing results to clinical outcome, plasma proteomics, and MASP2 expression. MASP2 plasma levels were 12.5-fold higher and MASP2 pulmonary deposition greater in long COVID vs. severe acute COVID-19. MVEC were exposed to long COVID plasmas +/- narsoplimab and caspase 8, a marker of cell activation and apoptosis linked to acute COVID-19 pathology, assessed. Narsoplimab suppressed caspase 8 induction. RNAseq identified pathways associated with this activity in long COVID, components of which were reflected by plasma proteomics. Our data, in the context of an early clinical trial in acute COVID-19, recommend exploration of narsoplimab in long COVID-19.

ORGANISM(S): Homo sapiens

PROVIDER: GSE343379 | GEO | 2026/08/17

REPOSITORIES: GEO

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