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Nanostring of sorted lung conventional dendritic cells (cDCs) 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) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk from ECs to conventional (c)DCs in vivo, we examined immune-specific transcriptional profiles from lung cDCs 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 cDCs 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 alveolar macrophage (AM) RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

ORGANISM(S): Mus musculus

PROVIDER: GSE79614 | GEO | 2018/03/10

REPOSITORIES: GEO

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Array of sorted lung conventional dendritic cells (cDCs) from cell-specific MyD88 KO at 0h and 6h 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) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk from ECs to conventional (c)DCs in vivo, we examined transcriptional profiles from lung cDCs sorted at baseline or 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 specific transcriptional changes in cDCs that were cell-intrinsic as well as resulting from in vivo crosstalk from ECs. We also observed 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, sorted alveolar macrophage RNA, and sorted cDC by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

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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

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 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).

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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

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 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).

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Expression data from lung CD11b+ conventional dendritic cells in the steady-state and following exposure to house dust mite allergens

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Mus musculus

Project description:Nanostring of sorted lung conventional dendritic cells (cDCs) from cell-specific MyD88 KO at 6h after in vivo sensitization with OVA/standard flagellin

| PRJNA316446 | ENA

RNA-seq data of intestinal epithelial cells and lamina propria dendritic cells

Project description:We report that Klebsiella pneumoniae promote Th1 cell induction in colon. To examine the influence of Klebsiella on colonic epithelial cells (ECs) and lamina propria CD11c+ dendritic cells (DCs), we performed RNA seq on them. Germ free mice were orally inoculated with Kp-2H7 or BAA-2552 and total RNA was isolated from colonic ECs and DCs 1 week after inoculation. Furthermore, we examined the involvement of TLRs in induction of Th1 cells using Myd88 KO, Trif KO, Myd88/Trif DKO mice. These deficient germ free mice were orally inoculated with Kp-2H7 and total RNA was isolated from colonic ECs 3 weeks after inoculation.

2017-10-20 | GSE101678 | GEO

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Project description:Array of sorted lung conventional dendritic cells (cDCs) from cell-specific MyD88 KO at 0h and 6h in vivo sensitization with OVA/standard flagellin

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Chronic OVA model

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