Six months after ICU discharge from severe ARDS secondary to COVID-19, patients with gas exchange impairment exhibit evidence of systemic inflammation, along with elevated ICAM-1 levels, ultimately resulting in increased plasma ET-1 levels.

The persistent systemic inflammation observed in these patients may be attributed to increased activity of the NLRP3 inflammasome, leading to an increase in inflammatory cytokines, exacerbated by T-cell activation.

Specifically, elevated levels of sCD40-L, along with persistent IFN-β-mediated viral inflammation, were observed. Both sCD40-L and IFN-β influenced endothelial function.

Collectively, these findings provide insight into how systemic inflammation contributes to endothelial dysfunction, impairing gas exchange and perpetuating this alteration, impacting patients’ symptomatology and quality of life months after acute infection.

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