| Literature DB >> 22047990 |
Naiara Miranda Rust1, Michelle Premazzi Papa, Aline Miranda Scovino, Mayara Marques Carneiro da Silva, Carlos Eduardo Calzavara-Silva, Ernesto Torres de Azevedo Marques, Ligia Maria Torres Peçanha, Julio Scharfstein, Luciana B Arruda.
Abstract
Sindbis virus (SINV) induces inflammatory and vasoactive responses that are associated with rash and arthritis in human infections. The mechanisms underlying infection-associated microvasculopathy are still unknown. We investigated whether endothelial cells infected by SINV are differentially responsive to bradykinin (BK), a potent inducer of inflammatory edema in a broad range of infectious diseases. Human endothelial cells (HBMECs) infected with SINV presented an upregulation of bradykinin B2 receptors (BK2R) expression. Also, BK reduced SINV-induced apoptosis and enhanced virus replication in HBMECs in a way dependent on BK2R, PI3 kinase and ERK signaling. Strikingly, intracerebral infection of mice in the presence of a BK2R antagonist reduced the local viral load. Our data suggest that SINV infection renders human endothelial cells hypersensitive to BK, which increases host cell survival and viral replication. Ongoing studies may clarify if the deregulation of the kinin pathway contributes to infection-associated vasculopathies in life-threatening arbovirus infections.Entities:
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Year: 2011 PMID： 22047990 DOI： 10.1016/j.virol.2011.10.003
Source DB: PubMed Journal: Virology ISSN： 0042-6822 Impact factor: 3.616