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Transcriptome Profiling of Influenza A Virus-infected Lung Epithelial (A549) Cells with Lariciresinol-4-β-D-glucopyranoside Treatment

ABSTRACT: The influenza A virus is an acute contagious pathogen that affects the human respiratory system and can cause severe lung disease and even death. Lariciresinol-4-β-D-glucopyranoside is a lignan that is extracted from Isatis indigotica, which is a medicinal herb plant that was commonly applied to treat infections, the common cold, fever and inflammatory diseases. Our previous study demonstrated that lariciresinol-4-β-D-glucopyranoside possesses anti-viral and anti-inflammatory properties. However, the comprehensive and detailed mechanisms that underlie the effect of lariciresinol-4-β-D-glucopyranoside interventions against influenza virus infection remain to be elucidated. In this study, we employed high-throughput RNA sequencing (RNA-seq) to investigate the transcriptomic responses of influenza A virus-infected lung epithelial (A549) cells with lariciresinol-4-β-D-glucopyranoside treatment. The transcriptome data show that infection with influenza A virus prompted the activation of 368 genes involved in RIG-I signalling, the inflammatory response, interferonsignalling and gene expression that was not affected by lariciresinol-4-β-D-glucopyranoside treatment. Lariciresinol-4-β-D-glucopyranoside exerted its pharmacological actions on the immune system, signal transduction, cell cycle and metabolism, which may be an underlying defence mechanism against influenza virus infection. In addition, 166 differentially expressed genes (DEGs) were uniquely expressed in lariciresinol-4-β-D-glucopyranoside-treated cells, which were concentrated in the cell cycle, DNA repair, chromatin organization, gene expression and biosynthesis domains. Among them, six telomere-associated genes were up-regulated by lariciresinol-4-β-D-glucopyranoside treatment, which have been implicated in telomere regulation and stability. Collectively, we employed RNA-seq analysis to provide comprehensive insight into the mechanism of lariciresinol-4-β-D-glucopyranoside against influenza virus infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE93999 | GEO | 2017/01/25

SECONDARY ACCESSION(S): PRJNA363033

REPOSITORIES: GEO

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Project description:Annually, influenza A viruses circulate the world causing wide-spread sickness, economic loss, and death. One way to better defend against influenza virus-induced disease may be to develop novel host-based therapies, targeted at mitigating viral pathogenesis through the management of virus-dysregulated host functions. However, mechanisms that govern aberrant host responses to influenza virus infection remain incompletely understood. We previously showed that the pandemic H1N1 virus influenza A/California/04/2009 (H1N1; CA04) has enhanced pathogenicity in the lungs of cynomolgus macaques relative to a seasonal influenza virus isolate (A/Kawasaki/UTK-4/2009 (H1N1; KUTK4)). Here, we used microarrays to identify host gene sequences that were highly differentially expressed (DE) in CA04-infected macaque lungs, and we employed a novel strategy M-bM-^@M-^S combining functional and pathway enrichment analyses, transcription factor binding site enrichment analysis and protein-protein interaction data M-bM-^@M-^S to create a CA04 differentially regulated host response network. This network describes enhanced viral RNA sensing, immune cell signaling and cell cycle arrest in CA04-infected lungs, and highlights a novel, putative role for the MYC-associated zinc finger (MAZ) transcription factor in regulating these processes. Lung tissues used for microarray studies were obtained from 13 female cynomolgus macaques infected with influenza viruses. 6 animals were inoculated with influenza A/California/04/2009 and 6 animals were inoculated with influenza A/Kawasaki/UTK-4/2009. 1 uninfected animal served as a negative control. On days 3 and 7 post-infection (p.i.), lung tissues were harvested from the middle and lower lung lobes of 3animals in each infection group (N = 26 total samples were collected, 3 samples were removed from the study due to low RNA quality). All but 3 samples were collected from visually apparent virus-induced gross lesions. Two lung tissue samples were obtained from middle and lower lobes of the uninfected animal at the start of the experiment.

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Transcriptome Profiling of Influenza A Virus-infected Lung Epithelial (A549) Cells with Lariciresinol-4-β-D-glucopyranoside Treatment

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