Dengue Virus Serotype-2 Interferes with the Formation of Neutrophil Extracellular Traps
2015; Karger Publishers; Volume: 58; Issue: 4 Linguagem: Inglês
10.1159/000440723
ISSN1423-0100
AutoresMaría Maximina Bertha Moreno‐Altamirano, Oscar Rodríguez‐Espinosa, O Rojas-Espinosa, Bernardo Pliego‐Rivero, Francisco Javier Sánchez‐García,
Tópico(s)Advanced Nanomaterials in Catalysis
Resumo<b><i>Objectives:</i></b> Neutrophils play an important role in the control of pathogens through several mechanisms, including phagocytosis and the formation of neutrophil extracellular traps (NETs). The latter consists of DNA as a backbone with embedded antimicrobial peptides, histones, and proteases, providing a matrix to entrap and in some cases to kill microbes. Some metabolic requirements for NET formation have recently been described. The virus-induced formation of NETs and the role of these traps in viral infections remain scarcely reported. Here, we analyzed whether dengue virus serotype-2 (DENV-2) induces NET formation and the DENV-2 effect on phorbol myristate acetate (PMA)-induced NETs. <b><i>Methods:</i></b> Peripheral blood-derived neutrophils were exposed in vitro to DENV-2 or exposed to DENV-2 and then stimulated with PMA. NET formation was assessed by fluorescence microscopy. Cell membrane Glut-1, glucose uptake, and reactive oxygen species (ROS) production were assessed. <b><i>Results:</i></b> DENV-2 does not induce the formation of NETs. Moreover, DENV-2 inhibits PMA-induced formation of NETs by about 80%. This effect is not related to the production of ROS. The mechanism seemingly accountable for this inhibitory effect is the DENV-2-mediated inhibition of PMA-induced glucose uptake by neutrophils. <b><i>Conclusion:</i></b> Our results suggest that DENV-2 inhibits glucose uptake as a metabolism-based way to avoid the formation of NETs.
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