Project description:Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness and remodeling. In this study, we aimed to investigate the transcriptomic changes in the lung tissue of asthmatic mice using a well-established ovalbumin (OVA)-induced asthma model. Female BALB/c mice (6-8 weeks old) were randomly divided into two groups: sham (n=6) and OVA (n=5). The OVA group received intraperitoneal injections of 20 μg OVA and 2 mg Al(OH)₃ on days 0 and 14. Subsequently, from day 21 to day 23, the mice were exposed to 1% OVA aerosol for 30 minutes each day. The sham group received an equivalent volume of vehicle. After 24 hours of the last aerosol exposure, the mice were sacrificed, and lung tissues were collected for RNA sequencing. The sequencing data were analyzed to identify differentially expressed genes and pathways associated with asthma development and progression. The results provide valuable insights into the molecular mechanisms underlying OVA-induced asthma and may identify potential therapeutic targets.
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. Thus, we hypothesis that asthmatic BSM cell metabolism is modified compare to that of non-asthmatic and that could be a potential target to reduce asthmatic BSM cell proliferation and remodeling in asthma.
Project description:Next generation sequencing (NGS) results demonstrate the modulative capacity of LCPUFAs on dysregulated miRNA expression in asthma. Methods: Sequencing of miRNA was performed by NGS from lung tissue of asthmatic and control mice with normal diet, as well as of LCPUFA supplemented asthmatic mice using Illumina miSeq. Conclusion: Our results demonstrate the modulative capacity of LCPUFAs on dysregulated miRNA expression in asthma.
Project description:The goal of the was to evaluate the mRNA expression profile of asthmatic and non-asthmatic airway smooth muscle using Next Generation Sequencing (RNA seq).
Project description:Obese asthma is a chronic disease that poses a serious threat to children's health, resulting in more severe wheezing, earlier airway remodelling, and insensitivity to hormone therapy. Despite its clinical importance, knowledge on the underlying mechanisms of this disease remains limited. This study aimed to elucidate the pathogenesis of obese asthmatic utilizing a murine model. The present study randomly divided thirty female BALB/c mice into three groups: normal mice, asthmatic mice, and obese asthmatic mice. The mice were fed a with high-fat diet (HFD) to induce obesity. Asthmatic mice were subjected to ovalbumin (OVA) sensitization and challenge. Mice with obesity were then subjected to OVA sensitization and challenge to develop obese asthmatic. Airway remodelling was observed in obese asthmatic mice. Proteomic and bioinformatics analyses were conducted on lung tissues from obese asthmatic and normal mice. A total of 200 proteins were differentially expressed in obese asthmatic compared to normal mice; of these, 53% were upregulated and 47% were downregulated. Pathway analysis revealed that obese asthmatic primarily affected the lysosome, phagosome, and sphingolipid metabolism pathways. In addition, pyroptosis was observed in obese asthmatic, along with significant increases in pyroptosis-related factors. Orosomucoid like 3 (ORMDL3), NOD-like receptor thermal protein domain associated protein 3 (NLRP3) and Gasdermin-D (GSDMD) expression was examined, with particularly high expression levels observed in obese asthmatic mice. In vitro experiments demonstrated that overexpression of ORMDL3 in human bronchial epithelial (HBE) cells led to increased expression of NLRP3, GSDMD, and cathepsin D (CTSD). These findings suggest that ORMDL3 may regulate pyroptosis and subsequent airway remodelling in obese asthmatic, possibly via CTSD/NLRP3/GSDMD pathway.
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. We thus hypothesis that asthmatic BSM cells could act on bronchial epithelium and modified its response to rhinovirus infection.