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Nanostring of whole lung RNA from cell-specific MyD88 KO at 0h, 2h and 6h after in vivo sensitization with OVA/standard flagellin

ABSTRACT: Allergic asthma is a chronic disease of the airways characterized by eosinophilic and neutrophilic inflammation. MYD88, the adaptor molecule for TLR and IL-1 family member signaling, is required for allergic sensitization through the airway in animal models of allergic asthma. We generated conditionally mutant mice separately lacking Myd88 in airway epithelial cells (ECs) or dendritic cells (DCs) and alveolar macrophages (AMs) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk between ECs and CD11c-expressing cells in vivo, we examined transcriptional profiles from whole lung RNA at baseline, or following 2h or 6h in vivo lung allergic sensitization through the airways from WT MyD88 fx/fx, SPC cre+ MyD88 fx/fx (EC-MYD88 KO), CD11c cre+ MyD88 fx/fx (DC-MYD88 KO), and full MyD88 KO mice. We observed immune-specific transcriptional changes in whole lung RNA that were altered based on EC- or CD11c-specific deletion of MYD88. We also observed transcriptional (linked data set) and epigenetic changes in chromatin conformation in cDCs by ATAC-seq (linked data set) as well as changes in immune-specific sorted EC RNA, sorted AM RNA, and sorted cDC RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

ORGANISM(S): Mus musculus

PROVIDER: GSE79594 | GEO | 2018/03/10

REPOSITORIES: GEO

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Nanostring of sorted lung alveolar macrophages (AM) from cell-specific MyD88 KO at 6h after in vivo sensitization with OVA/standard flagellin

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