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MYD88-dependent dendritic and epithelial cell crosstalk in the lung orchestrates immune responses to inhaled allergens

ABSTRACT: MYD88-dependent dendritic and epithelial cell crosstalk in the lung orchestrates immune responses to inhaled allergens

PROVIDER: PRJNA316442 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3216480_1.fastq.gz	Fastqsanger.gz
	SRR3216480_2.fastq.gz	Fastqsanger.gz
	SRR3216490_1.fastq.gz	Fastqsanger.gz
	SRR3216490_2.fastq.gz	Fastqsanger.gz
	SRR3216481_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

MyD88-dependent dendritic and epithelial cell crosstalk orchestrates immune responses to allergens.

Project description:Sensitization to inhaled allergens is dependent on activation of conventional dendritic cells (cDCs) and on the adaptor molecule, MyD88. However, many cell types in the lung express Myd88, and it is unclear how signaling in these different cell types reprograms cDCs and leads to allergic inflammation of the airway. By combining ATAC-seq with RNA profiling, we found that MyD88 signaling in cDCs maintained open chromatin at select loci even at steady state, allowing genes to be rapidly induced during allergic sensitization. A distinct set of genes related to metabolism was indirectly controlled in cDCs through MyD88 signaling in airway epithelial cells (ECs). In mouse models of asthma, Myd88 expression in ECs was critical for eosinophilic inflammation, whereas Myd88 expression in cDCs was required for Th17 cell differentiation and consequent airway neutrophilia. Thus, both cell-intrinsic and cell-extrinsic MyD88 signaling controls gene expression in cDCs and orchestrates immune responses to inhaled allergens.

| S-EPMC5918466 | biostudies-literature

MYD88-dependent dendritic and epithelial cell crosstalk in the lung orchestrates immune responses to inhaled allergens

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-03-10 | GSE79615 | GEO

Human plasma proteome changes during inhaled allergen challenge

Project description:Inhaled allergen challenge of subjects with allergic asthma allows the study of mechanisms involved in allergen-induced airway inflammation. The objective of this study was to identify changes in the plasma proteome associated with a late phase response (LPR) causing airway obstruction occurring 4-8 hours after the initial early response. Serial plasma samples from asthmatics undergoing inhaled allergen challenge were analyzed. Mass spectrometry data was analyzed using a linear regression to model the relationship between the degree of airway obstruction during the LPR and plasma proteome changes evoked by the inhaled allergen challenge. Inhaled allergen challenge induced changes in the plasma proteome including upregulation of the protease inhibitors alpha-1-antitrypsin, alpha-1-antichymotrypsin and plasma serine protease inhibitor. Out of 396 quantified proteins, 150 showed a statistically significant change 23 hours post allergen challenge. Further proteomic changes were associated with the LPR, including altered levels of coagulation factors such as an increased factor XII A and a decreased von Willebrand factor. Allergic reactions to inhaled allergens in asthmatic subjects was associated with changes in a large proportion of the measured plasma proteome, whereof protease inhibitors show the largest changes, likely to influence the inflammatory response. Of several other proteins altered in relation to the LPR, many are associated with coagulation.

2022-04-14 | PXD027091 | Pride

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).

2018-03-10 | GSE79592 | GEO

Nanostring of sorted lung conventional dendritic cells (cDCs) 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) 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).

2018-03-10 | GSE79614 | GEO

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).

2018-03-10 | GSE79581 | GEO

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).

2018-03-10 | GSE79591 | GEO

Keratinocyte-Macrophage Crosstalk by the Nrf2/Ccl2/EGF Signaling Axis Orchestrates Tissue Regeneration

Project description:Keratinocyte-Macrophage Crosstalk by the Nrf2/Ccl2/EGF Signaling Axis Orchestrates Tissue Regeneration

| PRJNA668615 | ENA

ATAC-seq of sorted lung cDCs (conventional dendritic cells) 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 epigenetic crosstalk from ECs to conventional (c)DCs in vivo, we examined ATAC-seq data 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 epigenetic changes in chromatin conformation in cDCs that were cell-intrinsic as well as resulting from in vivo crosstalk from ECs. We also observed transcriptional changes in cDCs by Affymetrix Whole Transcriptome Array (linked data set) as well as changes in immune-specific whole lung RNA, sorted EC RNA, sorted alveolar macrophage RNA, and sorted cDC RNA changes by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

2018-03-10 | GSE79062 | GEO

Commensal bacteria and the lung environment are responsible for Th2-mediated memory yielding natural IgE in MyD88-deficient mice

Project description:IgE antibody is known as a common mediator of allergic responses, generally produced in type 2 immune responses to allergens. It is known that IgE binding to FcεRI without allergen binding promotes survival or proliferation of mast cells, basophils and other cells. Thus, spontaneously produced IgE, namely natural IgE, can increase an individual’s susceptibility to allergic diseases. Mice with a genetic defect in MyD88, a major signaling molecule downstream of Toll-like receptors, have a high level of serum natural IgE, the mechanism for which remains unknown. Here, we demonstrated that the maintenance of high serum IgE levels depends on memory B cells (MBCs). IgE from plasma cells and the sera from most of Myd88–/– mice, but none of Myd88+/– mice, recognized Streptococcus azizii (S. azizii), a commensal bacterium over-represented in the lung of Myd88–/– mice. IgG1+ MBCs from spleen also recognized S. azizii. The serum IgE levels declined by administration of antibiotics and were boosted by challenge with S. azizii in Myd88–/– mice. Moreover, bulk IgH repertoire analysis revealed that CDR3 sequences were highly shared between IgE+ PCs and IgG1+ or IgG2+ MBCs, indicating the contribution of S. azizii-specific IgG1+ MBCs to the natural IgE production.

2023-01-27 | GSE220657 | GEO

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