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Transcriptomic analysis of lung tissue from WT mice treated with or without MSDC-0602K following influenza virus infection

ABSTRACT: To identify molecular characteristics of lung tissue from WT mice treated with DMSO or a new insulin sensitizer MSDC-0602K at day 4 post influenza virus infection, we isolated RNA from lungs with various treatments and examined by bulk RNA-seq. We found a large number of gene profiles were altered following MSDC-0602K treatment in lungs. Interestingly, gene sets involved inflammatory responses were enriched in DMSO treatd mouse lungs whereas gene set of fatty acid metabolism was enriched in MSDC-0602K treated mouse lung, suggesting MSDC-0602K treatment diminshed pulmonary inflammation and altered metabolic status during influenza virus infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE181776 | GEO | 2023/02/23

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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Transcriptomic analysis of lung tissue from WT mice treated with or without MSDC-0602K following influenza virus infection

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