tetano
Editor, Senior Moderator
Physiol Genomics. 2018 Jun 29. doi: 10.1152/physiolgenomics.00051.2018. [Epub ahead of print]
[h=1]Influenza virus infection modulates the death receptor pathway during early stages of infection in human bronchial epithelial cells.[/h] Othumpangat S[SUP]1[/SUP], Beezhold DH[SUP]2[/SUP], Noti JD[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Host-viral interaction occurring throughout the infection process between the influenza A virus (IAV) and bronchial cells determines the success of infection. Our previous studies showed that the apoptotic pathway triggered by the host cells was repressed by IAV facilitating prolonged survival of infected cells. A detailed understanding on the role of IAV in altering the cell death pathway during early stage infection of human bronchial epithelial cells (HBEpCs) is still unclear. We investigated the gene expression profiles of IAV-infected versus mock-infected cells at the early stage of infection using a PCR array for death receptor (DR) pathway. At early stages infection (2h) with IAV significantly upregulated DR pathway genes in HBEpCs, whereas 6h exposure to IAV resulted in downregulation of same genes. IAV replication in HBEpCs decreased the levels of DR pathway genes including TNF-receptor super family1, Fas-associated Death Domain, caspase-8, and caspase-3, by 6h, resulting in increased survival of cells. The apoptotic cell population decreased in 6h compared to the 2h exposure to IAV. The PCR array data was imported into Ingenuity pathway analysis software, resulting in confirmation of the model showing significant modulation of the DR pathway. Our data indicate that a significant transcriptional regulation of apoptotic, necrotic and DR genes occur at early and late hours of infection that are vital in modulating the survival of host cells and replication of IAV. These data intuitively may have provided a likely roadmap for translational approaches targeting the DR pathway to enhance apoptosis and inhibit replication of the virus.
[h=4]KEYWORDS:[/h] Death recepotor; apoptosis; caspase-8; influenza virus; lung epithelial cells
PMID: 29958081 DOI: 10.1152/physiolgenomics.00051.2018
[h=1]Influenza virus infection modulates the death receptor pathway during early stages of infection in human bronchial epithelial cells.[/h] Othumpangat S[SUP]1[/SUP], Beezhold DH[SUP]2[/SUP], Noti JD[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Host-viral interaction occurring throughout the infection process between the influenza A virus (IAV) and bronchial cells determines the success of infection. Our previous studies showed that the apoptotic pathway triggered by the host cells was repressed by IAV facilitating prolonged survival of infected cells. A detailed understanding on the role of IAV in altering the cell death pathway during early stage infection of human bronchial epithelial cells (HBEpCs) is still unclear. We investigated the gene expression profiles of IAV-infected versus mock-infected cells at the early stage of infection using a PCR array for death receptor (DR) pathway. At early stages infection (2h) with IAV significantly upregulated DR pathway genes in HBEpCs, whereas 6h exposure to IAV resulted in downregulation of same genes. IAV replication in HBEpCs decreased the levels of DR pathway genes including TNF-receptor super family1, Fas-associated Death Domain, caspase-8, and caspase-3, by 6h, resulting in increased survival of cells. The apoptotic cell population decreased in 6h compared to the 2h exposure to IAV. The PCR array data was imported into Ingenuity pathway analysis software, resulting in confirmation of the model showing significant modulation of the DR pathway. Our data indicate that a significant transcriptional regulation of apoptotic, necrotic and DR genes occur at early and late hours of infection that are vital in modulating the survival of host cells and replication of IAV. These data intuitively may have provided a likely roadmap for translational approaches targeting the DR pathway to enhance apoptosis and inhibit replication of the virus.
[h=4]KEYWORDS:[/h] Death recepotor; apoptosis; caspase-8; influenza virus; lung epithelial cells
PMID: 29958081 DOI: 10.1152/physiolgenomics.00051.2018