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10.1086/590499 http://scihub22266oqcxt.onion/10.1086/590499 18613795!ä!18613795 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18613795&cmd=llinks): Failed to open stream: HTTP request failed! 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Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection |pdf=|usr=}}{{18613795}} gab.com Text Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection JO: J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=18613795 #FOAvip The mechanism for the pathogenesis of H5N1 infection in humans remains unclear. This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease. Novel findings demonstrated that COX-2, along with tumor necrosis factor alpha and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro. This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade. These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs. Twit Text FOAVip Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection ????J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=18613795 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18613795 #FOAvip English Wikipedia <ref>{{Cite pmid|18613795}}</ref> Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection #MMPMID18613795 Lee SM; Cheung CY; Nicholls JM; Hui KP; Leung CY; Uiprasertkul M; Tipoe GL; Lau YL; Poon LL; Ip NY; Guan Y; Peiris JS J Infect Dis 2008[Aug]; 198 (4): 525-35 PMID18613795show ga The mechanism for the pathogenesis of H5N1 infection in humans remains unclear. This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease. Novel findings demonstrated that COX-2, along with tumor necrosis factor alpha and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro. This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade. These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs. |Animals[MESH] |Birds[MESH] |Cyclooxygenase 2 Inhibitors[MESH] |Cyclooxygenase 2/*biosynthesis/genetics[MESH] |Humans[MESH] |Influenza A Virus, H5N1 Subtype/genetics/*immunology/*pathogenicity[MESH] |Influenza in Birds/*enzymology/immunology/virology[MESH]Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a(epmc).pdf DeepDyve Pubget Overpricing