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- W4313386739 abstract "Abstract Highly pathogenic influenza viruses can elicit a severe cytokine storm, leading to acute lung injury (ALI), or in its more severe form, acute respiratory distress syndrome (ARDS). Reactive oxygen species (ROS) produced by NADPH Oxidase (Nox) enzymes of both the lung infiltrating cells and the lung epithelial tissue can contribute to lung injury directly or via inflammatory signaling pathways. Here, we present evidence that Nox1 expression is enhanced in vitro (A549 lung epithelial cells, 33-fold; THP-1 monocytic cells, 633-fold; HULEC lung endothelial cells, 27-fold) and in vivo (mouse lung tissue, 17-fold) in response to infection with influenza A virus. Notably, in A549 cells, Nox1 expression levels were enhanced by laboratory strains A/X31 (H3N2) and A/WSN/33 (H1N1), as well as A(H1N1)pdm09 clinical isolates (A/California/08/2009, A/Mexico/4108/2009, and A/Texas/15/2009) of influenza A virus. Nox1 induction was virus dose- and replication-dependent. However, Nox1-deficient mice had a higher survival rate (p=0.008) compared to wild-type controls in response to a lethal dose of A/PR8/1934 influenza. Improved survival of Nox1-deficient mice corresponded with increased (p=0.0006) flu-specific neutralizing antibody responses. These results suggest that therapeutic blockade of Nox1 deserves further attention as a possible adjunct therapy for influenza A-associated ALI/ARDS." @default.
- W4313386739 created "2023-01-06" @default.
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- W4313386739 date "2013-05-01" @default.
- W4313386739 modified "2023-09-26" @default.
- W4313386739 title "Adverse role of influenza A virus-induced Nox1 in neutralizing antibody responses and survival against lethal viral challenge in mice. (P1407)" @default.
- W4313386739 doi "https://doi.org/10.4049/jimmunol.190.supp.57.15" @default.
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