期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 18, 页码 -出版社
MDPI
DOI: 10.3390/ijms221810144
关键词
low type-2 asthma; obesity; asthma phenotypes; CD4(+) T cells; transcriptomics
资金
- German Center for Lung Research (DZL)
- German Academic Exchange Service (DAAD)
- HessenFonds, World University Service (WUS)
- Hessen State Ministry for Higher Education, Research and the Arts (HMWK)
- German Research Foundation (DFG) [512416910386GRK 2573/1]
In this study, RNA sequencing was conducted on peripheral blood CD4(+) T cells from obese non-atopic asthmatic adults, non-obese non-atopic asthmatic adults, and healthy controls. The results showed specific activation of interferon-related signaling pathways in obese asthmatics, while gap junction and GPCR ligand binding pathways were enriched in both asthma groups. Additionally, markers for obesity genes were upregulated in CD4(+) T cells from obese asthmatics, indicating potential novel targets for stratified therapeutic approaches.
In the era of personalized medicine, insights into the molecular mechanisms that differentially contribute to disease phenotypes, such as asthma phenotypes including obesity-associated asthma, are urgently needed. Peripheral blood was drawn from 10 obese, non-atopic asthmatic adults with a high body mass index (BMI; 36.67 +/- 6.90); 10 non-obese, non-atopic asthmatic adults with normal BMI (23.88 +/- 2.73); and 10 healthy controls with normal BMI (23.62 +/- 3.74). All asthmatic patients were considered to represent a low type-2 asthma phenotype according to selective clinical parameters. RNA sequencing (RNA-Seq) was conducted on peripheral blood CD4(+) T cells. Thousands of differentially expressed genes were identified in both asthma groups compared with heathy controls. The expression of interferon (IFN)-stimulated genes associated with IFN-related signaling pathways was specifically affected in obese asthmatics, while the gap junction and G protein-coupled receptor (GPCR) ligand binding pathways were enriched in both asthma groups. Furthermore, obesity gene markers were also upregulated in CD4(+) T cells from obese asthmatics compared with the two other groups. Additionally, the enriched genes of the three abovementioned pathways showed a unique correlation pattern with various laboratory and clinical parameters. The specific activation of IFN-related signaling and viral infection pathways might provide a novel view of the molecular mechanisms associated with the development of the low type-2 obesity-associated asthma phenotype, which is a step ahead in the development of new stratified therapeutic approaches.
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