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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

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 from ECs to AMs in vivo, we examined transcriptional profiles from lung AMs sorted following 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 AMs that were cell-intrinsic as well as resulting from in vivo crosstalk from ECs. 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 whole lung RNA, sorted EC RNA, and sorted cDC RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

ORGANISM(S): Mus musculus

PROVIDER: GSE79592 | GEO | 2018/03/10

REPOSITORIES: GEO

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Nanostring of sorted airway epithelial cells (AECs) from cell-specific MyD88 KO at 2h after in vivo sensitization with OVA/standard flagellin

Project description: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 from CD11c-expressing cells to ECs in vivo, we examined immune-specific transcriptional profiles from lung ECs sorted following 2h 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 ECs that were cell-intrinsic but none resulting from in vivo crosstalk from CD11c-expressing cells. 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 whole lung RNA, sorted AM RNA, and sorted cDC RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

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