Human airway inflammatory cell response to LPS and house dust mite antigen
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE5272 | GEO | 2009/10/01
SECONDARY ACCESSION(S): PRJNA96379
REPOSITORIES: GEO
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Project description:Allergic asthmatic, allergy only, asthma only (no allergy), and non-allergic non-asthmatic (control) subjects underwent bronchoscopy with instillation of saline, lipopolysaccharide (LPS), and house dust mite antigen in separate subsegmental bronchi. Airway epithelial cells were collected four hours later (three samples per subject). RNA was extracted from these cells for microarray analysis. Keywords: gene expression arrays (two-dye: sample against common "universal" reference RNA)
2009-10-01 | GSE8190 | GEO
Project description:Allergic asthmatic, allergy only, asthma only (no allergy), and non-allergic non-asthmatic (control) subjects underwent bronchoscopy with instillation of saline, lipopolysaccharide (LPS), and house dust mite antigen in separate subsegmental bronchi. Bronchoalveolar lavage (BAL) fluid was collected four hours later (three samples per subject). Inflammatory cells from each specimen were isolated and RNA was extracted for microarray analysis. Experiment Overall Design: There are four main phenotypic groups: Experiment Overall Design: 1. control (no allergy or asthma) Experiment Overall Design: 2. allergy only (no asthma) Experiment Overall Design: 3. asthma only (no allergy) Experiment Overall Design: 4. allergy and asthma Experiment Overall Design: and three exposures: saline, house dust mite antigen (HDM), and LPS. Experiment Overall Design: Samples from the different exposures were all collected at the same time: four hours after instillation. The hybridizations were carried out in two main 'batches': samples in batch 1 were processed in mid 2004, samples in batch 2 about a year later in 2005. There is a clear 'batch effect': differences between expression profiles from the two batches (likely caused by technical differences between hybridization and scanning methods). This should be considered when analyzing the data.
2009-10-10 | E-GEOD-5272 | biostudies-arrayexpress
Project description:Allergic asthmatic, allergy only, asthma only (no allergy), and non-allergic non-asthmatic (control) subjects underwent bronchoscopy with instillation of saline, lipopolysaccharide (LPS), and house dust mite antigen in separate subsegmental bronchi. Airway epithelial cells were collected four hours later (three samples per subject). RNA was extracted from these cells for microarray analysis. Experiment Overall Design: There are four main phenotypic groups: Experiment Overall Design: 1. control (no allergy or asthma) Experiment Overall Design: 2. allergy only (no asthma) Experiment Overall Design: 3. asthma only (no allergy) Experiment Overall Design: 4. allergy and asthma Experiment Overall Design: and three exposures: saline, house dust mite antigen (HDM), and LPS. Samples from the different exposures were all collected at the same time: four hours after instillation. The hybridizations were carried out in two main "batches": samples in batch 1 were processed in mid 2004, samples in batch 2 about a year later in 2005. There is a clear "batch effect": differences between expression profiles from the two batches (likely caused by technical differences between hybridization and scanning methods). This should be considered when analyzing the data.
2009-10-11 | E-GEOD-8190 | biostudies-arrayexpress
Project description:CD4 T cells are essential mediators of the asthmatic process. We used the clinically relevant allergen house dust mites to induce signs of allergy in mice and performed gene expression arrays specifically on CD4 T cells infiltrating the lung Reference: IL-21-producing CD4+ T cells promote type 2 immunity to house dust mites
2015-08-13 | GSE72005 | GEO
Project description:The increase in atopic diseases has occurred in such a short period of time that it becomes difficult to be attributed only to genetic factors, which usually need more prolonged time periods to manifest. In this setting during the last decade, the science of epigenetics has increasingly developed offering new perspectives and opening a new challenging research area. In this study we aimed to study the epigenetic patterns in B CD19+ Lymphocytes from healthy and allergic patients using the improved version of HELP assay. Our study focused specifically on DNA methylation in B CD19+ Lymphocytes isolated from whole blood of dust allergic patients (ALLERGY, n=3), aspirin intolerants (ASPIRIN INTOLERANT, n=3) and healthy subjects (CONTROL, n=3). We utilized a two-stage design involving genome-wide discovery followed by quantitative, single-locus validation. Each microarray consists of a two-color comparison of a methylation-sensitive representation of the genome (HpaII) with an internal methylation-insensitive control/reference (MspI).
2011-12-01 | E-GEOD-26080 | biostudies-arrayexpress
Project description:CD4 T cells are essential mediators of the asthmatic process. We used the clinically relevant allergen house dust mites to induce signs of allergy in mice and performed gene expression arrays specifically on CD4 T cells infiltrating the lung Reference: IL-21-producing CD4+ T cells promote type 2 immunity to house dust mites Primary CD4+ T cells were isolated from mice sensitised and challenged to either house dust mites or PBS. Purification of CD4 T cells was performed by flow cytometry. RNA was isolated, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 2.0 ST Arrays
2015-08-13 | E-GEOD-72005 | biostudies-arrayexpress
Project description:While the pathogenesis of asthma is mainly orchestrated by antigen-specific Th2 cells and their cytokines, recent findings indicate the involvement of other subsets of helper T cells including Th17 cells. Previous studies have shown that IL-22, one of Th17 cell-related cytokines, plays multiple roles in regulating allergic airway inflammation; however, the mechanism underlying the Il-22-mediated regulation remains unclear. Here, we show that allergic airway inflammation upon intratracheal administration of house dust mite extract (HDM), a representative allergen, were exacerbated in IL-22-deficient mice. To address the molecular mechanisms by which IL-22 inhibits the development of HDM-induced allergic airway inflammation, we next performed an unbiased comprehensive screening of genes induced by IL-22 administration in the lung by RNA-seq analysis.
2017-08-10 | GSE100858 | GEO
Project description:Despite robust literature associating IL-31 with pruritic inflammatory skin diseases, its influence on cutaneous inflammation and on the interplay between inflammatory and neurosensory pathways remain unmapped. Here, we examined the consequences of disrupting Il31 and its receptor Il31ra in a mouse model of house dust mite (HDM) allergic dermatitis. Il31-deficient mice displayed an increased number and proportion of cutaneous type 2 cytokine-producing CD4 T cells and serum IgE in response to HDM. Single cell RNA-sequencing analysis of skin CD45+ populations from HDM-treated skin revealed that Il4ra+ monocytes and macrophages capable of fueling a feedforward type 2 inflammatory loop were selectively enriched in Il31ra-deficient HDM dermatitis skin. Thus, IL-31 is not strictly a pro-inflammatory cytokine, but rather an immunoregulatory factor that limits the magnitude of type 2 inflammatory responses in skin.
2023-10-26 | GSE236744 | GEO
Project description:Purpose: Identify whole lung gene expression patterns modified by nanoparticle delivery of an antisense LNA/DNA oligonucleotide targeting mmu-miR145a-5p and nontargeting oligonucleotides Methods: Lung gene expression profiles of 10 week old BALB/c female mice were generated by polyA RNA-seq with Illumina HiSeq v4. Sequence reads that passed quality filters after timming were analyzed at the gene level with RNA STAR, featureCounts and Deseq2 . qRT–PCR validation was performed using TaqMan and SYBR Green methods. Results: 10-15 million sequence reads per sample were mapped to the mouse genome (build mm10). Pathway analysis of differentially expressed genes identified upregulation of gene sets for human asthma, mouse lung allergic inflammation, Muc5ac regulated genes and smooth muscle genes after allergic sensitization. Gene level exppression in each asthma-related pathway was reduced by the miR-145 antagonist. The miR-145 antagonist and several nontargeting oligos also upregulated interferon signaling pathways suggesting a general antiinflammatory effect of LNA/DNA oligos in the lung. Conclusions: Lung-directed delivery of LNA/DNA oligonucleotides with cationic lipid nanoparticles is an efffective means to prevent inflammatory gene expression in a house dust mite model of asthma
2019-02-16 | GSE126610 | GEO
Project description:This study aims to investigate the role and mechanism of DEK in asthmatic airway inflammation and in regulating PTEN-induced putative kinase 1 (PINK1)-Parkin mediated mitophagy, NLRP3 (NOD-like receptor family pyrin domain containing 3) inflammasome activation, and apoptosis. We found that recombinant DEK protein (rmDEK) promoted eosinophils recruitment, mitochondrial fragmentation, and outer membrane 20 (TOM20) and LC3 co-localization representing mitophagosomes in bronchoalveolar lavage fluid (BALF) in house dust mite (HDM) induced-asthma. rmDEK also reduced co-localization of mitochondrial fusion protein mitofusin1 (MFN1) and mitochondria, and the protein level of manganese superoxide dismutase (MnSOD), enhanced microtubule-associated protein1 light chain 3 (LC3) and voltage-dependent anion channels (VDAC) co-localization which also represent the mitophagosomes in airway epithelial cells, furthermore, increased dynamin-related protein 1 (DRP1) expression, PINK1-Parkin-mediated mitophagy, NLRP3 inflammasome activation, and apoptosis. In the DEK knockout mice, HDM induced asthmatic airway inflammation, MnSOD, PINK1-Parkin protein level, Parkin mediated mitophagy characterized by LC3 and Parkin co-localization in the airways, ROS generation, NLRP3 inflammation and apoptosis were fully reversed. Similar effects of rmDEK were also observed in the BEAS-2B cells, which were rescued by the autophagy inhibitor 3-MA. Moreover, DEK silencing diminished the Parkin, LC3, DRP1 translocation to mitochondria; as well as mitochondrial ROS; TOM20 and mitochondrial DNA mediated mitochondrial oxidative damage. ChIP-sequence analysis showed that DEK was enriched on the AAA domain-containing protein 3A (ATAD3A) promoter and could positively regulate ATAD3A expression. Additionally, ATAD3A was highly expressed in HDM-induced asthma models. Furthermore, ATAD3A interacted with DRP1, and knockdown of ATAD3A could down-regulate DRP1 and mitochondrial oxidative damage. Conclusively, DEK deficiency alleviates airway inflammation in asthma by down-regulating PINK1-Parkin mitophagy, NLRP3 inflammasome activation, and apoptosis. The mechanism may be through the DEK/ATAD3A/DRP1 signaling axis. Our findings may provide new potential therapeutic targets for asthma treatment.
2023-09-24 | GSE243532 | GEO