COVID-19 is the syndrome caused by SARS-CoV-2 infection. Severe phenotypes seem to be caused by a “cytokines storm” and pneumonia is one of the most important clinical features. COVID-19 could also be a trigger for fibrotic abnormalities. Initially, we compared patients at hospitalization and healthy controls, focusing on acute phase biomarkers, especially IL-32, IL-8, IL-6 and IL-10. 64 patients underwent blood sample at hospitalization and 27 healthy controls were also included. The serum concentrations of IL-1β, IL-10, IFN-γ, TNF-α, IL-6, IL-8 and IL-32 were assessed. IL-8 was higher in COVID-19 patients than in controls, on the contrary IL-32 was lower. IL-6 was higher in patients with severe COVID-19, instead IL-10 was lower in this group. Then, we evaluated a set of adipokines and cytokines in 108 hospitalized patients stratified according to clinical severity. 56 of them also underwent radiological and spirometry follow-up 3-6 months after discharge. Concerning the severity of disease, we found higher levels of TGF- β and IL-6 and lower levels of RBP-4 and IL-10 in the severe group. Subsequent analysis revealed that vaccinated patients showed higher levels of MCP-1 and IL-10. Considering the risk of fibrosis development, we observed higher levels of IL-1β, IL17A, TNF-α, TGF-β, IL-4 and IL-6 at hospitalization in the group with fibrotic alterations at follow-up. Regarding spirometry at follow-up, FVC% correlated inversely with TNF-α and directly with IL-32. Finally, we chose a population of 89 follow-up patients previously hospitalized for COVID-19. Samples were collected during follow-up visits. The follow-up protocol included medical examination, HRCT of the chest, blood tests and lung function tests. The clinical data and medical history, also concerning the acute phase of COVID-19, were available for 80/89 patients. Severity of COVID-19 during hospitalization was recorded. Presence of fibrotic abnormalities did not affect spirometry values, but only DLCO. Direct comparison of cytokine levels in the two groups exhibited increased levels of IL-32 and decreased levels of IL-8 in patients with lung fibrotic alterations. IL-10 emerged as the only cytokine persistently decreased in previously severe patients.
Bianchi, F. (2024). Biomarkers in COVID-19 pandemic: implications for acute phase assessment and chronic management [10.25434/bianchi-francesco_phd2024-03-20].
Biomarkers in COVID-19 pandemic: implications for acute phase assessment and chronic management
bianchi francesco
2024-03-20
Abstract
COVID-19 is the syndrome caused by SARS-CoV-2 infection. Severe phenotypes seem to be caused by a “cytokines storm” and pneumonia is one of the most important clinical features. COVID-19 could also be a trigger for fibrotic abnormalities. Initially, we compared patients at hospitalization and healthy controls, focusing on acute phase biomarkers, especially IL-32, IL-8, IL-6 and IL-10. 64 patients underwent blood sample at hospitalization and 27 healthy controls were also included. The serum concentrations of IL-1β, IL-10, IFN-γ, TNF-α, IL-6, IL-8 and IL-32 were assessed. IL-8 was higher in COVID-19 patients than in controls, on the contrary IL-32 was lower. IL-6 was higher in patients with severe COVID-19, instead IL-10 was lower in this group. Then, we evaluated a set of adipokines and cytokines in 108 hospitalized patients stratified according to clinical severity. 56 of them also underwent radiological and spirometry follow-up 3-6 months after discharge. Concerning the severity of disease, we found higher levels of TGF- β and IL-6 and lower levels of RBP-4 and IL-10 in the severe group. Subsequent analysis revealed that vaccinated patients showed higher levels of MCP-1 and IL-10. Considering the risk of fibrosis development, we observed higher levels of IL-1β, IL17A, TNF-α, TGF-β, IL-4 and IL-6 at hospitalization in the group with fibrotic alterations at follow-up. Regarding spirometry at follow-up, FVC% correlated inversely with TNF-α and directly with IL-32. Finally, we chose a population of 89 follow-up patients previously hospitalized for COVID-19. Samples were collected during follow-up visits. The follow-up protocol included medical examination, HRCT of the chest, blood tests and lung function tests. The clinical data and medical history, also concerning the acute phase of COVID-19, were available for 80/89 patients. Severity of COVID-19 during hospitalization was recorded. Presence of fibrotic abnormalities did not affect spirometry values, but only DLCO. Direct comparison of cytokine levels in the two groups exhibited increased levels of IL-32 and decreased levels of IL-8 in patients with lung fibrotic alterations. IL-10 emerged as the only cytokine persistently decreased in previously severe patients.File | Dimensione | Formato | |
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https://hdl.handle.net/11365/1257154