tetano
Editor, Senior Moderator
Front Physiol. 2017 Feb 14;8:89. doi: 10.3389/fphys.2017.00089. eCollection 2017.
[h=1]Prostaglandin E2 As a Modulator of Viral Infections.[/h] Sander WJ[SUP]1[/SUP], O'Neill HG[SUP]1[/SUP], Pohl CH[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Viral infections are a major cause of infectious diseases worldwide. Inflammation and the immune system are the major host defenses against these viral infection. Prostaglandin E[SUB]2[/SUB] (PGE[SUB]2[/SUB]), an eicosanoid generated by cyclooxygenases, has been shown to modulate inflammation and the immune system by regulating the expression/concentration of cytokines. The effect of PGE[SUB]2[/SUB] on viral infection and replication is cell type- and virus-family-dependent. The host immune system can be modulated by PGE[SUB]2[/SUB], with regards to immunosuppression, inhibition of nitrogen oxide (NO) production, inhibition of interferon (IFN) and apoptotic pathways, and inhibition of viral receptor expression. Furthermore, PGE[SUB]2[/SUB] can play a role in viral infection directly by increasing the production and release of virions, inhibiting viral binding and replication, and/or stimulating viral gene expression. PGE[SUB]2[/SUB] may also have a regulatory role in the induction of autoimmunity and in signaling via Toll-like receptors. In this review the known effects of PGE[SUB]2[/SUB] on the pathogenesis of various infections caused by herpes simplex virus, rotavirus, influenza A virus and human immunodeficiency virus as well the therapeutic potential of PGE[SUB]2[/SUB] are discussed.
[h=4]KEYWORDS:[/h] immunity; inflammation; prostaglandin E2; therapeutic agents; viral infection
PMID: 28261111 DOI: 10.3389/fphys.2017.00089
[PubMed - in process] Free full text
[h=1]Prostaglandin E2 As a Modulator of Viral Infections.[/h] Sander WJ[SUP]1[/SUP], O'Neill HG[SUP]1[/SUP], Pohl CH[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Viral infections are a major cause of infectious diseases worldwide. Inflammation and the immune system are the major host defenses against these viral infection. Prostaglandin E[SUB]2[/SUB] (PGE[SUB]2[/SUB]), an eicosanoid generated by cyclooxygenases, has been shown to modulate inflammation and the immune system by regulating the expression/concentration of cytokines. The effect of PGE[SUB]2[/SUB] on viral infection and replication is cell type- and virus-family-dependent. The host immune system can be modulated by PGE[SUB]2[/SUB], with regards to immunosuppression, inhibition of nitrogen oxide (NO) production, inhibition of interferon (IFN) and apoptotic pathways, and inhibition of viral receptor expression. Furthermore, PGE[SUB]2[/SUB] can play a role in viral infection directly by increasing the production and release of virions, inhibiting viral binding and replication, and/or stimulating viral gene expression. PGE[SUB]2[/SUB] may also have a regulatory role in the induction of autoimmunity and in signaling via Toll-like receptors. In this review the known effects of PGE[SUB]2[/SUB] on the pathogenesis of various infections caused by herpes simplex virus, rotavirus, influenza A virus and human immunodeficiency virus as well the therapeutic potential of PGE[SUB]2[/SUB] are discussed.
[h=4]KEYWORDS:[/h] immunity; inflammation; prostaglandin E2; therapeutic agents; viral infection
PMID: 28261111 DOI: 10.3389/fphys.2017.00089
[PubMed - in process] Free full text