Post-COVID symptoms are reported in 10-35 % of patients not requiring hospitalization, and in up to 80 % of hospitalized patients and patients with severe disease. The pathogenesis of post-COVID syndrome remains largely unknown. Some evidence suggests that prolonged inflammation has a key role in the pathogenesis of most postCOVID manifestations. We evaluated a panel of inflammatory and immune-mediated cytokines in individuals with altered HRCT features and in patients without any long-term COVID symptoms. Blood samples of 89 adult patients previously hospitalized with COVID-19 were collected and stratified as patients with and without HRCT evidence of fibrotic lung alterations. Serum analyte concentrations of IL-4, IL-2, CXCL10 (IP-10), IL-1 beta, TNF-alpha, CCL2 (MCP-1), IL-17A, IL-6, IL-10, IFN-gamma, IL-12p70 and TGF-beta 1 (free active form) were quantified by bead-based multiplex assay. Clinical and functional data were recorded in a database. With the use of machine learning approach, IL-32, IL-8, and IL-10 proved to be associated with the development of HRCT evidence of lung sequelae at follow-up. Direct comparison of cytokine levels in the two groups showed increased levels of IL-32 and decreased levels of IL-8 in patients with lung impairment. After further stratification of patients by severity (severe versus mild/moderate) during hospitalization, IL-10 emerged as the only cytokine showing decreased levels in severe patients. These findings contribute to a better understanding of the immune response and potential prognostic markers in patients with lung sequelae after COVID-19.

Bergantini, L., Gangi, S., D'Alessandro, M., Cameli, P., Perea, B., Meocci, M., et al. (2024). Altered serum concentrations of IL-8, IL-32 and IL-10 in patients with lung impairment 6 months after COVID-19. IMMUNOBIOLOGY, 229(4) [10.1016/j.imbio.2024.152813].

Altered serum concentrations of IL-8, IL-32 and IL-10 in patients with lung impairment 6 months after COVID-19

Bergantini, Laura;Gangi, Sara;d'Alessandro, Miriana;Cameli, Paolo;Perea, Beatrice;Meocci, Martina;Fabbri, Gaia;Bianchi, Francesco;Bargagli, Elena
2024-01-01

Abstract

Post-COVID symptoms are reported in 10-35 % of patients not requiring hospitalization, and in up to 80 % of hospitalized patients and patients with severe disease. The pathogenesis of post-COVID syndrome remains largely unknown. Some evidence suggests that prolonged inflammation has a key role in the pathogenesis of most postCOVID manifestations. We evaluated a panel of inflammatory and immune-mediated cytokines in individuals with altered HRCT features and in patients without any long-term COVID symptoms. Blood samples of 89 adult patients previously hospitalized with COVID-19 were collected and stratified as patients with and without HRCT evidence of fibrotic lung alterations. Serum analyte concentrations of IL-4, IL-2, CXCL10 (IP-10), IL-1 beta, TNF-alpha, CCL2 (MCP-1), IL-17A, IL-6, IL-10, IFN-gamma, IL-12p70 and TGF-beta 1 (free active form) were quantified by bead-based multiplex assay. Clinical and functional data were recorded in a database. With the use of machine learning approach, IL-32, IL-8, and IL-10 proved to be associated with the development of HRCT evidence of lung sequelae at follow-up. Direct comparison of cytokine levels in the two groups showed increased levels of IL-32 and decreased levels of IL-8 in patients with lung impairment. After further stratification of patients by severity (severe versus mild/moderate) during hospitalization, IL-10 emerged as the only cytokine showing decreased levels in severe patients. These findings contribute to a better understanding of the immune response and potential prognostic markers in patients with lung sequelae after COVID-19.
2024
Bergantini, L., Gangi, S., D'Alessandro, M., Cameli, P., Perea, B., Meocci, M., et al. (2024). Altered serum concentrations of IL-8, IL-32 and IL-10 in patients with lung impairment 6 months after COVID-19. IMMUNOBIOLOGY, 229(4) [10.1016/j.imbio.2024.152813].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/1268255