Cell Type-Specific Mechanisms of Interleukin-8 Induction by Dengue Virus and Differential Response to Drug Treatment

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Abstract

In vitro infection with dengue virus induces interleukin (IL)-8 secretion, which increases endothelial cell permeability; this has been proposed as a mechanism for plasma leakage in dengue hemorrhagic fever. We studied the mechanisms of IL-8 induction, using luciferase reporter constructs, and the effect of pharmacological inhibitors of either IL-8 secretion or nuclear factor-κB (NF-κB) activation on IL-8 induction by dengue 2 virus (DEN2V) infection. IL-8 induction by DEN2V infection was associated with activation of NF-κB and activator protein-1 (AP-1) in HEK293A cells but only with activation of AP-1 in HepG2 cells. Treatment with SB203580, a mitogen-activated protein kinase inhibitor, and rolipram, a phosphodiesterase IV inhibitor, partially inhibited DEN2V-induced IL-8 secretion in HEK293A cells but increased DEN2V-induced IL-8 secretion in HepG2 cells. In contrast, treatment with dexamethasone increased DEN2V-induced IL-8 secretion in HEK293A cells but had no effect on DEN2V-induced IL-8 secretion in HepG2 cells. These results demonstrate that anti-inflammatory drugs have variable effects on IL-8 secretion in different cell types during DEN2V infection

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