Dataset related to the article "Low-grade inflammation in Long-COVID syndrome sustains a persistent platelet activation associated with lung impairment"

This record contains raw data related to the article "Low-grade inflammation in Long-COVID syndrome sustains a persistent platelet activation associated with lung impairment" ABSTRACT Background_Long-COVID syndrome is characterized by symptoms persisting after acute infection remission. In acute COVID-19 patients, platelets show a proinflammatory/prothrombotic phenotype. Whether this phenotype can sustain the residual pulmonary impairment observed in Long-COVID patients has yet to be established. Objective_To characterize platelet activation persistence, the underlying mechanisms, and the possible relationship with pulmonary function 6-months after acute COVID-19 remission. Methods_Among 204 enrolled subjects with a 6-month follow-up post-SARS-CoV-2 infection, 34 patients reporting symptoms of Long-COVID were compared with 34 COVID-Recovered and 34 healthy subjects (HS). Platelet activation (P-selectin, Tissue Factor, platelet-monocyte and platelet-granulocyte aggregates [PMA and PGA]) profiles were analyzed by flow-cytometry. Plasma levels of C-reactive protein (CRP) and Interleukin-6 (IL-6), lung diffusion (DLNO) and pulmonary CT scan were evaluated. Results_Seven-fold higher CRP levels were measured in Long-COVID compared to COVID-Recovered subjects. The percentage of PGA and PMA, which was persistently greater in Long-COVID than in COVID-Recovered patients and HS (1.5-fold), correlated with CRP levels (r=0.43,p=0.035; r=0.42,p=0.033; respectively), residual lung damage (r=0.55,p=0.004; r=0.54,p=0.006, respectively) and DLNO (r=0.16,p=0.036; r=0.24,p=0.049, respectively). Plasma from Long-COVID patients mixed with plasma-depleted HS blood induced P-selectin expression and platelet-leukocyte aggregate formation through a CRP- and IL-6-dependent mechanism, which are hallmarks prevented by Fcγ-receptor inhibitor, tocilizumab, aspirin and P2Y12 antagonist. Conclusions_Low-grade inflammation in Long-COVID patients sustains a pro-inflammatory platelet phenotype that significantly correlates with residual parenchymal damage. In ex vivo experiments, Long-COVID plasma reproduces the platelet activation observed in vivo. This effect is blunted by antiinflammatory and antiplatelet drugs, suggesting a potential therapeutic option in this clinical setting. This dataset is not public. It’s available upon reasonable requesto to the corresponding author.