medwireNews: Rheumatoid arthritis (RA) and COVID-19 pneumonitis share some common pathogenic pathways that could be targeted in the development of treatment strategies for COVID-19, researchers report.
Using publicly available datasets, Mariola Kurowska-Stolarska (University of Glasgow, UK) and team found that genetically determined macrophage clusters that are predominant in bronchoalveolar lavage fluid from patients with severe COVID-19 (FCN1+ and FCN1+SPP1+) are “transcriptionally related” to two synovial tissue macrophage clusters (CD48hiS100A12+ and CD48+SPP1+) known to drive synovitis in RA.
They also showed that plasma concentrations of the associated proteins – SPP1 (osteopontin) and S100A12 (calgranulin C) – were significantly higher among 92 hospitalized patients with acute COVID-19 compared with 10 healthy controls and 41 patients with prior SARS-CoV-2 infection who were in the convalescence phase.
In the COVID-19 patients, plasma SPP1 and S100A12 remained significantly higher than normal for at least 10 weeks after SARS-CoV-2 infection clearance, and further investigation into SPP1’s mechanism of action showed that it induced proinflammatory CD14+ monocyte activation.
“Thus, COVID-19 pneumonitis appears driven by similar pathogenic myeloid cell pathways as those in RA, and their mediators such as SPP1 may be an upstream activator of the aberrant innate response in severe COVID-19 and predictive of disease trajectory including post–COVID-19 monitoring,” write the researchers in JCI Insight.
“Promising data from current COVID-19 clinical trials of drugs already used for the treatment of RA (e.g., dexamethasone, tocilizumab, and baricitinib) further support the concept of common pathogenic and resolution mechanisms that could be capitalized upon for COVID-19 therapeutic exploitation,” they add.
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