Assuntos
Betacoronavirus/isolamento & purificação , Pérnio/diagnóstico , Infecções por Coronavirus/complicações , Pneumonia Viral/complicações , Pele/imunologia , Urticária/diagnóstico , Betacoronavirus/genética , Betacoronavirus/imunologia , Biópsia , COVID-19 , Teste para COVID-19 , Pérnio/imunologia , Pérnio/patologia , Pérnio/virologia , Técnicas de Laboratório Clínico , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/virologia , Diagnóstico Diferencial , Feminino , Humanos , Pessoa de Meia-Idade , Nasofaringe/virologia , Pandemias , Pneumonia Viral/diagnóstico , Pneumonia Viral/virologia , Reação em Cadeia da Polimerase , RNA Viral , SARS-CoV-2 , Pele/patologia , Pele/virologia , Urticária/imunologia , Urticária/patologia , Urticária/virologiaRESUMO
Stimulating monocytes/macrophages with bacterial lipopolysaccharide (LPS) results in TNF-alpha, IL-1, IL-6 and nitrite (NO2-) formation. Inhibitors of poly(ADP-ribose)polymerase inhibit release of these mediators by preventing mRNA expression indicating that ADP-ribosylation plays a crucial role in the synthesis of these mediators. Furthermore we present evidence that ADP-ribosylation is involved in modifying cellular proteins. In murine macrophages a 33 kDa cytosolic protein could be identified that in response to LPS changed its state of ADP-ribosylation, and in human monocytes we showed that the inhibitor nicotinamide prevents LPS induced phosphorylation of two cytosolic proteins of 36 kDa and 38 kDa (p36/38) LPS. Taken together these data indicate that protein modification by ADP-ribosylation may control cellular processes involved in distinct steps of monocyte/macrophage activation.
