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I've posted this sort of thing in the "HIV/AIDS" debate thread, but I think this deserves its own thread:
QUOTE: Numerous reports have described modulatory effects of viruses or proteins of the viral envelopes on the arachidonic acid (AA) cascade. For example, Behera et al. [19] reported that respiratory syncytial virus (RSV) infection of a bronchial epithelial cell line leads to an up-regulation of the biosynthesis of LTs. These results were consistent with other findings showing that increased LT synthesis correlated with the presence of RSV particles in patients affected with pneumonia or bronchiolitis [20,21]. Exposure of monocytic cells to the HIV-1 glycoprotein gp120 induced the expression of cyclooxygenase and lipoxygenase pathway enzymes [22], and it was reported recently that the cytotoxic effect of gp120 on a neuroblastoma cell line involved activation of the AA cascade together with enhanced membrane lipid peroxidation [23]. We have described previously the capacity of EBV to prime monocytes for an increased synthesis of LTB4 and LTC4 through modulation of 5-LO activity [24]. In the present study, we show that exposure of PMN to EBV enhances levels of LTB4 biosynthesis upon stimulation with a second agonist through a mechanism implicating a direct stimulatory effect of EBV on cPLA2 phosphorylation (Ser-505) and a priming effect of the viral particles on the translocation of cPLA2 induced by neutrophil agonists. Since phagocytes play a crucial role in host defence against infectious agents, changes in the generation of proinflammatory mediators may be an important issue in the early events of viral infection... UNQUOTE.
Source: Clin Exp Immunol. 2001 December; 126(3): 494�?02.
On the internet:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1906243
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