In December 2019, a novel coronavirus, “SARS-CoV-2”, was recognized as the cause of coronavirus disease 2019 (COVID-19). Several studies have explored the changes and the role of inflammatory cells and cytokines in the immunopathogenesis of the disease, but until today, the results have been controversial. Based on these premises, we conducted a retrospective assessment of monocyte intracellular TNF-α expression (iTNF-α) and on the frequencies of lymphocyte sub-populations in twenty-five patients with moderate/severe COVID-19. We found lymphopenia in all COVID-19 infected subjects compared to healthy subjects. On initial observation, in patients with favorable outcomes, we detected a high absolute eosinophil count and a high CD4+/CD8+ T lymphocytes ratio, while in the Exitus Group, we observed high neutrophil and CD8+ T lymphocyte counts. During infection, in patients with favorable outcomes, we observed a rise in the lymphocyte count, in the monocyte and in Treg lymphocyte counts, and in the CD4+ and in CD8+ T lymphocytes count but a reduction in the CD4+/CD8+ T lymphocyte ratio. Instead, in the Exitus Group, we observed a reduction in the Treg lymphocyte counts and a decrease in iTNF-α expression. Our preliminary findings point to a modulation of the different cellular mediators of the immune system, which probably play a key role in the outcomes of COVID-19.

Clinical outcome prediction in COVID-19 patients by lymphocyte subsets analysis and monocytes’ iTNF-α expression / Madonna, G.; Sale, S.; Capone, M.; De Falco, C.; Santocchio, V.; Di Matola, T.; Fiorentino, G.; Pirozzi, C.; D'Antonio, A.; Sabatino, R.; Atripaldi, L.; Atripaldi, U.; Raffone, M.; Curvietto, M.; Grimaldi, A. M.; Vanella, V.; Festino, L.; Scarpato, L.; Palla, M.; Spatarella, M.; Perna, F.; Cerino, P.; Botti, G.; Parrella, R.; Montesarchio, V.; Ascierto, P. A.; Atripaldi, L.. - In: BIOLOGY. - ISSN 2079-7737. - 10:8(2021). [10.3390/biology10080735]

Clinical outcome prediction in COVID-19 patients by lymphocyte subsets analysis and monocytes’ iTNF-α expression

Grimaldi A. M.;Scarpato L.;Perna F.;Botti G.;Ascierto P. A.;
2021

Abstract

In December 2019, a novel coronavirus, “SARS-CoV-2”, was recognized as the cause of coronavirus disease 2019 (COVID-19). Several studies have explored the changes and the role of inflammatory cells and cytokines in the immunopathogenesis of the disease, but until today, the results have been controversial. Based on these premises, we conducted a retrospective assessment of monocyte intracellular TNF-α expression (iTNF-α) and on the frequencies of lymphocyte sub-populations in twenty-five patients with moderate/severe COVID-19. We found lymphopenia in all COVID-19 infected subjects compared to healthy subjects. On initial observation, in patients with favorable outcomes, we detected a high absolute eosinophil count and a high CD4+/CD8+ T lymphocytes ratio, while in the Exitus Group, we observed high neutrophil and CD8+ T lymphocyte counts. During infection, in patients with favorable outcomes, we observed a rise in the lymphocyte count, in the monocyte and in Treg lymphocyte counts, and in the CD4+ and in CD8+ T lymphocytes count but a reduction in the CD4+/CD8+ T lymphocyte ratio. Instead, in the Exitus Group, we observed a reduction in the Treg lymphocyte counts and a decrease in iTNF-α expression. Our preliminary findings point to a modulation of the different cellular mediators of the immune system, which probably play a key role in the outcomes of COVID-19.
2021
Clinical outcome prediction in COVID-19 patients by lymphocyte subsets analysis and monocytes’ iTNF-α expression / Madonna, G.; Sale, S.; Capone, M.; De Falco, C.; Santocchio, V.; Di Matola, T.; Fiorentino, G.; Pirozzi, C.; D'Antonio, A.; Sabatino, R.; Atripaldi, L.; Atripaldi, U.; Raffone, M.; Curvietto, M.; Grimaldi, A. M.; Vanella, V.; Festino, L.; Scarpato, L.; Palla, M.; Spatarella, M.; Perna, F.; Cerino, P.; Botti, G.; Parrella, R.; Montesarchio, V.; Ascierto, P. A.; Atripaldi, L.. - In: BIOLOGY. - ISSN 2079-7737. - 10:8(2021). [10.3390/biology10080735]
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/867979
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 3
  • ???jsp.display-item.citation.isi??? 3
social impact