IMEX   05356
INSTITUTO DE MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Neutrophil-Coxsackievirus interaction
Autor/es:
DENISE KVIATCOVSKY; MIRTA SCHATTNER; LEONARDO RIVADENEYRA; R.M. GOMEZ; SILVIA DE LA BARRERA
Lugar:
Mar del Plata
Reunión:
Congreso; LXI Reunión Científica Anual de Sociedad Argentina de Investigación Clínica; 2016
Institución organizadora:
Sociedad Argentina de Investigación Clínica
Resumen:
Coxsackieviruses B (CVBs) belong to the genus Enterovirus within the Picornaviridae family. After infection by the oral route and before viremia, CVBs replicate in lymphoid tissues, such as the tonsils and the Peyer?s patches. This early interaction with immune cells has been poorly studied. In this work, we focused in the CVB-neutrophil (Neu) interaction in order to clarify the role of these inflammatory cells in the CVB infection.For this aim, Neu were incubated with CVB and one day later viral RNA and infectious virus were searched in cells and supernatants. RT-PCR and flow cytometry (FC) studies, showed the presence of both, viral RNA and antigen in Neu-infected cell pellets. Infectivity assays confirmed the presence of infectious viral particles in the supernatants.To determine whether this Neu-CVB interaction triggered cell activation we first analyzed expression of CD11b. FC analysis showed increased levels of this adhesion cell receptor that correlated with and augmented Neu adhesion to extracellular matrix proteins such as fibrinogen and fibronectin (acid phosphatase activity).Observation of nuclear morphological changes by fluorescence microscopy and FC showed that apoptosis was significantly lower in infected cells compared to control samples. This increase of cell survival might be due to the release of proinflammatory cytokines by Neu-infected cells. In this regard, increased levels of IL-6, IL-1b and TNF-a production (ELISA) were detected in CVB-Neu supernatants. Moreover, these supernatants also showed increased chemoattractant (boyden chamber technique) and myeloperoxidase activity (ELISA).The interaction of CVB-Neu induced low levels of neutrophil extracellular traps (NETs) that were significantly potentiated in the presence of TNF-a.Our results indicate that interaction of Neu-CVB results in Neu activation and increased cell survival. This activation may play an important role in the subsequent pathogenesis of CVB infection.