Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chemical allergen-induced perturbations of the mouse lymph node DNA methylome

ABSTRACT: Epigenetic regulation of gene expression plays a pivotal role in the orchestration of immune responses and may determine the vigor, quality, or longevity of such responses. Chemical allergens can be divided into two categories: skin sensitizing chemicals associated with allergic contact dermatitis, and chemicals that cause sensitization of the respiratory tract and occupational asthma. In mice these are characterized by different T helper (Th) cell responses. To explore the regulation and maintenance of these divergent responses, mice were exposed to 2,4-dinitrochlorobenzene (DNCB; a contact allergen) or trimellitic anhydride (TMA; a respiratory allergen). DNA from draining lymph nodes was processed for methylated DNA immunoprecipitation (MeDIP) followed by hybridization to a whole-genome DNA promoter array. 6319 differently methylated regions (DMR) were identified following DNCB treatment, while 2178 DMRs were measured following TMA treatment, with approximately half of the TMA DMR common to DNCB. When limited to promoter region-associated DMR, 637 genes were uniquely associated with DNCB induced DMR but only 164 genes were unique to TMA DMR. Promoter-associated DMR unique to either DNCB or TMA were generally hypomethylated whereas DMR common to both allergens tended to be hypermethylated. Pathway analyses highlighted a number of immune related pathways, including chemokine and cytokine signalling. These data demonstrate that chemical allergen exposure results in characteristic patterns of DNA methylation indicative of epigenetic regulation of the allergic response.

ORGANISM(S): Mus musculus

PROVIDER: GSE54768 | GEO | 2014/02/07

SECONDARY ACCESSION(S): PRJNA237583

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Chemical allergen-induced perturbations of the mouse lymph node DNA methylome

Project description:Epigenetic regulation of gene expression plays a pivotal role in the orchestration of immune responses and may determine the vigor, quality, or longevity of such responses. Chemical allergens can be divided into two categories: skin sensitizing chemicals associated with allergic contact dermatitis, and chemicals that cause sensitization of the respiratory tract and occupational asthma. In mice these are characterized by different T helper (Th) cell responses. To explore the regulation and maintenance of these divergent responses, mice were exposed to 2,4-dinitrochlorobenzene (DNCB; a contact allergen) or trimellitic anhydride (TMA; a respiratory allergen). DNA from draining lymph nodes was processed for methylated DNA immunoprecipitation (MeDIP) followed by hybridization to a whole-genome DNA promoter array. 6319 differently methylated regions (DMR) were identified following DNCB treatment, while 2178 DMRs were measured following TMA treatment, with approximately half of the TMA DMR common to DNCB. When limited to promoter region-associated DMR, 637 genes were uniquely associated with DNCB induced DMR but only 164 genes were unique to TMA DMR. Promoter-associated DMR unique to either DNCB or TMA were generally hypomethylated whereas DMR common to both allergens tended to be hypermethylated. Pathway analyses highlighted a number of immune related pathways, including chemokine and cytokine signalling. These data demonstrate that chemical allergen exposure results in characteristic patterns of DNA methylation indicative of epigenetic regulation of the allergic response. Comparison of methylation profiles from allergens 2,4-dinitrochlorobenzene (DNCB; a contact allergen) and trimellitic anhydride (TMA; a respiratory allergen) or vehicle acetone:olive oil (AOO).

2014-02-07 | E-GEOD-54768 | biostudies-arrayexpress

A T cell-IL-3 axis controls the responsiveness of sensory neurons to allergens

Project description:In naïve individuals, sensory neurons directly detect and respond to allergens, leading both to the sensation of itch and the activation of local innate immune cells, which initiate the allergic immune response1,2. In the setting of chronic allergic inflammation, immune factors prime sensory neurons, causing pathologic itch3-7. While these bidirectional neuroimmune circuits drive responses to allergens, whether immune cells regulate the set-point for neuronal activation by allergens in the naïve state is unknown. Here we describe a T cell-IL-3 signaling axis that controls the allergen responsiveness of cutaneous sensory neurons. We define a poorly characterized epidermal T cell subset8, termed GD3 cells, that produces its hallmark cytokine IL-3 to promote allergic itch and the initiation of the allergic immune response. Mechanistically, IL-3 acts on Il3ra-expressing sensory neurons in a JAK2-dependent manner to lower their threshold for allergen activation without independently eliciting itch. This T cell-IL-3 signaling axis further acts via STAT5 to promote neuropeptide production and the initiation of allergic immunity. These results reveal an endogenous immune rheostat that sits upstream of and governs sensory neuronal responses to allergens upon first exposure. This pathway may explain individual differences in allergic susceptibility and opens novel therapeutic avenues for treating allergic diseases.

2024-06-11 | GSE223220 | GEO

Allergen-induced vital DNA release by the airway epithelium amplifies type-2 immunity

Project description:This study has several novel aspects that address molecular mechanisms underlying type 2 immunity and allergic inflammation. We have identified a previously unknown response of human airway epithelial cells to allergens that involves rapid mobilization and release of nuclear DNA (nDNA) from epithelial cells that remain viable throughout the duration of exposure. We show that nDNA release occurs across the apical membrane, but not the basolateral membrane and that sequence analysis of the secreted DNA reveals proportionally higher amounts of promotor and exon sequences and lower intron and intergenic sequences compared to the normal distributions of these regions in the intact genome. Furthermore, unlike DNA release during NETosis, the extracellular DNA is highly fragmented, ranging in size from 1000-5000 bp. We discovered that allergen exposure stimulates caspase 3 by a non-canonical mechanism involving calcium-dependent activation of furin and that caspase 3 activity leads to DNA fragmentation as shown in comet assays. Using a mouse model of allergic inflammation, we demonstrate that allergen-induced type 2 immune responses are markedly reduced by pretreatment with a DNA scavenger and that nDNA release was significantly reduced in mice that were caspase 3 deficient. Moreover, we show that intranasal treatment with mouse genomic DNA combined with submaximal exposure to allergens amplified secretion of Th2 cytokines into bronchoalveolar lavage fluid while DNA alone had no effect. These results highlight a novel, allergen-dependent mechanism of regulated and rapid nDNA mobilization and release that amplifies type 2 immunity in airways and suggests that pharmacotherapies targeting this mechanism may be beneficial in reducing allergic inflammation and exacerbation of asthma.

2022-10-01 | GSE198721 | GEO

Project description:Allergen exposure was thought to play a critical role in the etiology of AR. And allergen avoidance, the practice of avoiding exposure to allergens, has been generally advised as the management of AR. However, the effect is uncertain and the underlying mechanism is far from known. We used gene expression microarrays to identify genes differentially regulated by allergen avoidance in allergic rhinitis mouse model.

2013-11-28 | GSE52804 | GEO

Molecular profiling of contact dermatitis skin identifies allergen-dependent differences in immune response

Project description:Different allergens induce different immune responses genomic profiling of specific allergen obtained after patched tests in skin

2014-08-02 | E-GEOD-60028 | biostudies-arrayexpress

Allergens Elicit an Antiviral Signature in Dendritic Cells

Project description:This study compares the transcriptomic changes induced by three distinct aeroallergens in a dendritic cell line with the goal of finding similarities in the response at the gene expression level. Using RNA sequencing of DC2.4 cells, we find that house dust mite, cat hair and timothy grass allergen extracts all induce what appears to be an antiviral genetic signature despite the lack of any viral components in each allergen. Such information may be useful in trying to design therapeutics or interventions for allergic responses which could be effective for multiple allergens despite differences in source and structure.

2021-08-20 | GSE182277 | GEO

Allergen detection in commercial foods

Project description:The frequent use of precautionary food allergen labeling statements such as “may contain” poses challenges to allergic individuals relying on such labeling to determine whether a food is safe to consume. To survey the frequency at which these precautionary statements indicate allergen contamination in commercial foods we developed a multiplexed liquid chromatography-mass spectrometry assay targeting 14 common allergens. For each allergen, we selected two or more tryptic peptides belonging to two or more clinically-recognized allergenic proteins by following one of two approaches. For certain allergenic proteins, a wealth of existing mass spectrometry literature suggests ideal tryptic peptide targets. In these cases, such for milk proteins Bos d 5 and Bos d 9, as well as peanut protein Ara h 3, we chose peptides using the Allergen Peptide Browser (APB), a freely available online database we developed. To choose peptides for the remaining allergenic proteins, as well as validate our choices, we applied shotgun proteomics to pure allergen protein extracts of the aforementioned allergens.

2019-07-17 | PXD007688 | Pride

Discovery-driven target selection from six milk-derived ingredients for consensus detection of casein and whey milk allergens

Project description:Milk is one among the most common food allergens and the proteins representing caseins and whey fractions of milk have been characterized as the major triggers for allergic responses in susceptible individuals. Milk or milk-derived ingredients- varying in their casein and whey protein content and composition- are present as an ingredient in many foods. This project was designed to identify candidate target peptides for casein and whey fractions of milk which can be used for milk allergen detection from foods irrespective of the type of ingredients used in them.

2020-06-05 | PXD016429 | Pride

Expression data from naive, effector and memory-like ILC2s isolated from mouse lungs and those from effector and memory-like ILC2s isolated from mediastinal lymph node

Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naÃ¯ve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens. ILC2s were isolated from mouse lungs from naive and IL-33 injected mice 4 days, 14 days and 4 months after the initial treatment. RNA was extracted from those ILC2 populations and analyzed for gene expression profiles. RNA was also extracted from ILC2s isolated from lung draining mediastinal lymph node (mLN) 4 days and 14 days after IL-33 treatment.

2016-06-30 | E-GEOD-81700 | biostudies-arrayexpress

Expression data from naive, effector and memory-like ILC2s isolated from mouse lungs and those from effector and memory-like ILC2s isolated from mediastinal lymph node

Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naïve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens.

2016-06-30 | GSE81700 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data