Human metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA434133 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10501800_1.fastq.gz | Fastqsanger.gz | |||
| SRR10501800_2.fastq.gz | Fastqsanger.gz | |||
| SRR10501900_1.fastq.gz | Fastqsanger.gz | |||
| SRR10501900_2.fastq.gz | Fastqsanger.gz | |||
| SRR10502000_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Obesity-associated asthma is recognized as a distinct entity with non-atopic T-helper 1 polarized systemic inflammation. DNA methylation is linked with T helper cell maturation and is associated with inflammatory patterns in asthma and obesity. However, it is unknown whether pathologic dysregulation of DNA methylation patterns occurs in obesity-associated asthma. Using HELP-tagging, we studied epigenome wide DNA methylation in peripheral blood mononuclear cells in 8 urban minority obese asthmatic pre-adolescent children and compared it to methylation in groups of 8 children with asthma alone, obesity alone and healthy controls. Ingenuity Pathway Analysis was used to identify biological pathways that were differentially targeted by methylation dysregulation. We found that obese asthmatics had distinct epigenome wide methylation patterns associated with decreased promoter methylation of a subset of genes, including RANTES, IL-12R and TBX21 and increased promoter methylation of CD23, a low affinity receptor for IgE and of TGFM-NM-2, inhibitor of Th cell activation. T cell signaling and macrophage activation were the two primary pathways that were selectively hypomethylated in obese asthmatics. These methylation patterns suggest that methylation is associated with non-atopic inflammation observed in obese asthmatic children compared to children with asthma alone and obesity alone. Our findings suggest a role of DNA methylation in the observed inflammatory patterns in pediatric obesity-associated asthma in minorities. 32 HpaII test
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Project description:Probiotic supplementation of overweight and obese adults
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