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Ad-MyD88 infected MEFs: Control vs. Ad-MyD88 infected

ABSTRACT: Transcriptional profiling of Murine Embryonic Fibroblasts (MEFs) infected with Ad-MyD88 vs. Ad-GFP or mock infected.

ORGANISM(S): Mus musculus

PROVIDER: GSE18957 | GEO | 2010/01/29

SECONDARY ACCESSION(S): PRJNA120993

REPOSITORIES: GEO

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Ad-MyD88 infected MEFs: Control vs. Ad-MyD88 infected

Project description:Transcriptional profiling of Murine Embryonic Fibroblasts (MEFs) infected with Ad-MyD88 vs. Ad-GFP or mock infected. Three-condition experiment, Ad-MyD88 vs. Ad-GFP vs. Mock infected cells. Biological replicates: 3 Ad-MyD88, 3 Ad-GFP, 3 mock, independently grown and harvested. One replicate per array.

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The in vivo cellular response to adenovirus and its regulation through MyD88

Project description:While recent studies of immunity have uncovered many aspects of the innate immune system, there has been precious little investigation of the cellular response to viruses in vivo. To this end, we exploited high titer adenoviral (Ad) vectors to investigate the cellular response to non-enveloped viral infection in vivo. Our results indicate a potent cellular transcriptome response early after infection, with global assessments revealing significant dysregulation in ~15% of measured transcripts derived from Ad infected tissue. Transcriptome analysis revealed a complex interplay between the innate and adaptive responses, with suppression of metabolism and mitochondrial genes akin to those observed when mice are challenged with LPS. But despite this common response profile, there were many unique aspects of the Ad dependent trancriptome response, including upregulation of several RNA regulatory mechanisms and apoptosis-related pathways, accompanied by suppression of lysosome, endocytic, Wnt, and Calcium signaling pathways. Investigations into the TLR pathway using MyD88KO mice revealed that Ad induction of the TLR, MAPK, and cytokine receptor genes are significantly dependent on MyD88, as well as five other functional gene modules (mitochondrial, RNA regulation, cell cycle and growth, extracellular, and immune response genes). Absence of MyD88 also resulted in a greatly diminished Th1 response and acute phase response at later time points, confirming the important role MyD88 plays as an anti-adenoviral immunity amplifier and regulator in vivo. However, continued activation of immune response genes in Ad infected MyD88KO mice indicates that MyD88 is not the only component of the Ad ‘sensing mechanism’ in vivo. Keywords: Infectious response, pathogen response

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Project description:Chlamydia pneumoniae, an obligate intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule MyD88 play a critical role in inducing immunity against this microorganism and are crucial to survive the infection. To explore the influence of MyD88 on induction of immune responses in vivo on a genome wide level, WT or MyD88-/- mice were infected with C. pneumoniae upon anesthesia and the pulmonary transcriptome was analyzed three days later by microarrays. We find that the infection induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88-/- mice. This cluster contains primarily genes encoding for chemokines, cytokines and other immune effector molecules. Genes induced by interferons were abundant in a cluster of 102 genes which were only partially MyD88-dependent. Interestingly, a set of 37 genes were induced more strongly in MyD88-/- mice and most of them are involved in the regulation of cellular replication. In summary, ex vivo analysis of the pulmonary transcriptome upon infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses, and identified MyD88-independent genes involved in cellular replication Experiment Overall Design: Microarray analysis was performed in biological triplicates with RNA from individual mice derived from three independent infection experiments. Samples were lungs from wt and myd88 knock out mice, three days after Chlamydia pneumoniae or mock infection. Altogther 12 samples were analyzed on Affymetrix MOE430A arrays.

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