Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of whole lungs from Irgm1-/- and wildtype littermates mice that were either uninfected or infected with influenza for 3, 6, or 10 days


ABSTRACT: We found that a dose of influenza (5,000 pfu of recombinant influenza A/WSN/33 (rWSN) H1N1 virus strain) that resulted in 50% mortality in wildtype littermate control mice showed minimal mortality in Irgm1-/- mice, indicating that Irgm1 deficiency was protective during influenza infection. This protective effect was dependent on the Type I interferon receptor Ifnar. We performed transcriptional profiling to identify molecular mechanisms associated with protection from influenza infection in Irgm1-/- lung. Both male and female mice were used at 8-12 weeks of age. Lung gene expression was assessed by RNA-seq at the following times post-influenza infection: Day 3 (early time point, early histological damage present in control mice), Day 6 (intermediate time point, late histological damage present in control mice) and Day 10 (late time point, morbidity and mortality present in control mice).

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Thaddeus Stappenbeck 

PROVIDER: E-MTAB-5337 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


The microbiota is known to modulate the host response to influenza infection through as-yet-unclear mechanisms. We hypothesized that components of the microbiota exert effects through type I interferon (IFN), a hypothesis supported by analysis of influenza in a gain-of-function genetic mouse model. Here we show that a microbially associated metabolite, desaminotyrosine (DAT), protects from influenza through augmentation of type I IFN signaling and diminution of lung immunopathology. A specific h  ...[more]

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