Project description:MiRNAs are involved in the pathogenesis of bronchial asthma and are involved in the regulation of airway inflammation, airway remodeling and airway hyperreactivity. In this experiment, we constructed OVA asthma model and identified the differentially expressed miRNAs in asthma and normal models by microarray technology, providing a preliminary basis for future studies on the mechanism of asthma. We used microarrays to detail the global program of gene expression in asthma models and identify miRNAs that are differentially expressed in this process.
Project description:Challenge with ovalbumin antigen is a common model for asthma in mice. We sought to identify the gene expression differences in lung tissue in naïve and OVA-sensitized mice, in response to OVA challenge.
Project description:The objective of the study was to present a transcriptome-wide m6A methylome profile of lung tissues in mouse model of ovalbumin(OVA)-induced acute allergic asthma.
Project description:Purpose: Identify genes disregulated in Balb mouse lung tissue in the Ovalbumin (OVA) asthma disease model and genes disregulated by OVA challenged mice treated with with an Anti-mouse-IL-4Ra mAb
Project description:Asthma bronchiale is an inflammatory disease of the respiratory airways and a major factor of increasing health care costs worldwide. The molecular actors leading to asthma are not fully understood and require further investigation. The aim of this study was to monitor the proteome during asthma development from early inflammatory to late fibrotic stages. A time-course-based ovalbumin (OVA) mouse model was applied to establish an asthma phenotype and the lung proteome was analysed at four time points during asthma development (0 weeks = control, 5 weeks, 8 weeks and 12 weeks of OVA treatment).
Project description:This program aims at identifying the lung gene signature associated with OVA-challenged mouse asthma model to facilitate understanding of the disease mechanism and therapeutic compound testing
Project description:This program aims at identifying the lung gene signature associated with OVA-challenged mouse asthma model to facilitate understanding of the disease mechanism and therapeutic compound testing The OVA-challenged profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the lungs of OVA-challenged mice compared to the corresponding PBS-treated controls.
Project description:Photobiomodulation (PBM) is a non-invasive therapeutic strategy that uses specific light wavelengths to stimulate cellular processes that promote tissue repair, reduce inflammation, and alleviate pain. In this study, we evaluated the efficacy of a high-intensity 980 nm near-infrared (NIR) pulsed laser in a murine model of ovalbumin (OVA)-induced allergic asthma. In OVA-sensitized mice, typical allergic features were noted, including airway wall thickening, significant peribronchial and perivascular inflammatory cell infiltration, and compressed alveolar spaces. NIR PBM treatment markedly attenuated these histological changes. At the molecular level, PBM significantly downregulated type 2 cytokine gene expression, including IL-4, IL-5 and IL-13, in the lung tissue. Flow cytometry analyses further revealed that PBM reduced the infiltration of pulmonary eosinophils and inflammatory monocytes. Transcriptomic profiling coupled with gene set enrichment analysis (GSEA) indicated that PBM suppressed NF-κB-mediated inflammatory signaling while modulating Th2-related responses. Collectively, our findings demonstrate that high-intensity 980 nm NIR PBM effectively mitigates key features of allergic asthma in a murine model, supporting its potential as a non-pharmacological, non-invasive adjunct therapy for asthma management.
Project description:Atopic asthma is a chronic inflammatory disease of the lungs that is commonly associated with a Th2 response. The role of allergen-specific IgG in the initiation and development of allergic airway inflammation is still poorly understood; however, a receptor of IgG-immune complexes, CD16, has been demonstrated to promote augmentation of Th2 responses. To identify what genes downstream of CD16 signaling may be contributing to development of a Th2 response, we use ovalbumin (OVA) as our model antigen and compared wildtype and CD16-/- BMDCs that were treated overnight with OVA or OVA-immune complex. C57Bl/6 and CD16-/- BMDCs were treated for 24 hours with OVA or OVA-immune complex and then analyzed for gene expression changes.
Project description:CpG-oligodeoxynucleotides (CpG-ODNs) constitute an attractive alternative for asthma treatment. We found that free feeding of an ODNcap (a CpG-ODN-embedded particle) -containing feed (ODNcap-F) prophylactically attenuates allergic airway inflammation, hyperresponsiveness, and goblet cell hyperplasia in an ovalbumin (OVA) -induced asthma model. To seek the suppressive mechanism of action of ODNcap-F in OVA-induced airway insults, we analyzed the lung transcriptome using DNA microarray analysis.