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10.1086/590499

http://scihub22266oqcxt.onion/10.1086/590499
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18613795!ä!18613795

suck abstract from ncbi


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pmid18613795      J+Infect+Dis 2008 ; 198 (4): 525-35
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  • 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]


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