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- W202326482 abstract "Abstract Avian influenza virus (AIV) H9N2 subtype has circulated in wild birds and domestic poultry, has successfully crossed the species boundary to transmit to and infect humans and have contributed to the generation of highly pathogenic H5N1 viruses. Little is known about host responses to H9N2 viruses in human airway respiratory epithelium. We used apically differentiated primary human tracheobronchial epithelial (hTBE) cultures to study host antiviral and apoptotic responses to an H9N2 virus strain. Compared to the immortalized bronchial epithelial cells HBE1, differentiated hTBE were less susceptible to the H9N2 virus. Among the antiviral cytokines, IFN-β was the prominent antiviral component in primary cultures. We found that IL-6, TNF-α, IP10 and CCL5 seemed to play important roles in proinflammatory responses while IL-1β and CCL5 were downregulated in primary hTBE cells. The AIV H9N2 virus caused apoptosis in both HBE1 and primary hTBE cultures. In addition to the extrinsic apoptotic pathway, we found that the mitochondria-mediated intrinsic cascade participated in H9N2-induced apoptosis, demonstrated by the cytosolic presence of active caspase 9 and cytochrome c. Further, our data indicated that FLIP and Bcl-2 family members Bax and Bcl-Xs appeared to be involved in the apoptotic regulation. The findings will further our understanding on host defense mechanisms and pathogenesis in human respiratory epithelium infected with AIV H9N2 virus." @default.
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- W202326482 date "2009-04-01" @default.
- W202326482 modified "2023-09-26" @default.
- W202326482 title "Host Immune and Apoptotic Responses to Low Pathogenic Avian Influenza Virus H9N2 in Human Tracheobronchial Epithelial Cells (130.15)" @default.
- W202326482 doi "https://doi.org/10.4049/jimmunol.182.supp.130.15" @default.
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