ABSTRACT: Expression data from lungs of Vldlr-/- mice and wild type (WT) B6129SF2/J mice that had received intranasal house dust mite (HDM) challenges to induce experimental asthma or saline, as a control.
Project description:Transcription profiling by array of lungs of Vldlr-/- mice and wild type (WT) B6129SF2/J mice that had received intranasal house dust mite (HDM) challenges to induce experimental asthma or saline
Project description:The very low density lipoprotein receptor (VLDLR) is a multi-ligand receptor that mediates pleiotropic biological processes, such as brain development. In this dataset, we include the expression data obtained from lungs from mice that had been challenged with house dust mite to induce experimental asthma or saline, as a control. These data are used to obtain genes that are differentially expressed in response to VLDLR signaling. We compared wild type and VLDLR knock out mice that had been sensitized and challenged with house dust mite or saline, as a control. There were total 16 samples with four biological relicates in each group.
Project description:The aim of this study was to investigate differential expression in a house dust mite (HDM) exposure model of asthma in rhesus macaques. HDM sensitization was performed by subcutaneous injection of HDM followed by intranasal HDM for 2-3 hours twice a week.
Project description:The aim of this study was to investigate differential expression in a house dust mite (HDM) exposure model of asthma in rhesus macaques. HDM sensitization was performed by subcutaneous injection of HDM followed by intranasal HDM for 2-3 hours twice a week. Animals were mock-sensitized (PBS) or sensitized to HDM antigen. Gene expression was measured in lung biopsies before and fifteen weeks after treatment.
Project description:We examined the transcriptional changes in mouse lungs induced by house dust mite (HDM), D.f. extract and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that HDM strongly triggered an inflammatory response.
Project description:This study are compares the transcriptomes of lower airway constitutive connective tissue mast cells (MCs), characterized by low expression of b7 integrin (B7low), and induced mucosal MCs, characterized by high b7 integrin (B7hi) at rest and in response to repeated inhalation of house dust mite extract (HDM). Lower airway b7hi and b7low MCs were flow cytometrically isolated from female 5-7 week old C57BL/6 mice following 6 challenges (2x/week for three weeks) with saline (PBS) or 3 ug house dust mite extract (HDM). Each sample is derived from pooled lung digests from three mice to reduce experimental variance. Samples were sequenced on an Illumina NextSeq 500
Project description:The very low density lipoprotein receptor (VLDLR) is a multi-ligand receptor that mediates pleiotropic biological processes, such as brain development. In this dataset, we include the expression data obtained from lungs from mice that had been challenged with house dust mite to induce experimental asthma or saline, as a control. These data are used to obtain genes that are differentially expressed in response to VLDLR signaling.
Project description:Levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, are increased in lung, sputum, exhaled breath condensate and plasma samples from asthma patients. ADMA is metabolized primarily by dimethylarginine dimethylaminohydrolase 1 (DDAH1) and DDAH2. We determined the effect of DDAH1 overexpression on development of allergic inflammation in mouse models of asthma. Wild type and DDAH1-transgenic mice were challenged with PBS or house dust mite (HDM). Airway inflammation was assessed by bronchoalveolar lavage (BAL) total and differential cell counts. Gene expression in lungs was determined by RNA-Seq and RT-quantitative PCR (qPCR). The expression of DDAH1 and DDAH2 was decreased in the lungs of mice following HDM exposure. Transgenic overexpression of DDAH1 resulted in decreased BAL total cell and eosinophil numbers following HDM exposure. Total IgE levels in serum and BAL fluid were decreased in HDM-exposed DDAH1-transgenic mice compared to HDM-exposed wild type mice. RNA-Seq results showed downregulation of genes in inducible nitric oxide synthase (iNOS) signaling pathway in PBS-treated DDAH1 transgenic mice versus PBS-treated wild type mice and downregulation of genes in IL-13/FOXA2 signaling pathway in HDM-treated DDAH1 transgenic mice versus HDM-treated wild type mice. Our findings suggest that decreased expression of DDAH1 in airway epithelial cells may contribute to allergic asthma and overexpression of DDAH1 attenuates allergen-induced airway inflammation through modulation of Th2 responses. mRNA profiles of WT and DDAH1-transgenic mice treated with PBS or house dust mite (HDM).
Project description:House dust mite (HDM) extract (Greer Laboratories, Lenoir, NC) was resuspended in sterile phosphate-buffered saline (PBS) at a concentration of 0.5 mg (protein)/ml and 10 ul (5 ug dose) was administered to isofluorane-anesthetized mice intranasally. Groups of mice were infected either with influenza A or exposed to PBS. Seven days later, separate groups of mice were either exposed to saline or HDM for 3 or 6 days and lungs harvested 24 h after the last exposure, at day 4 (early phase; EP) or day 7 (late phase; LP).
Project description:Using mouse lung resident conventional CD11b+ dendritic cells (CD11b+ cDCs) in the context of house-dust mite (HDM)-driven allergic airway sensitization as a model, we aimed here to identify transcriptional events regulating the pro-Th2 activity of cDCs. We used microarray analyses to identify genes differentially expressed by lung CD11b+ conventional dendritic cells in response to house dust mite allergens in wild-type and Irf3-deficient mice
