Exercise induced Selenbp1 targeting of macrophage M1 polarization in the development of obesity related asthma in children

Background: Childhood obesity and asthma represent significant worldwide public health challenges with disproportionate impacts on pediatric populations. Pediatric patients with comorbid obesity and asthma frequently demonstrate exacerbated clinical manifestations encompassing heightened immunological activation, dysregulated metabolic pathways, and chronic respiratory tract inflammation. Macrophage polarization, particularly the M1 phenotype, is crucial in the development of obesity-related asthma. Methods: Transcriptome microarray data relevant to obesity, asthma, and exercise were extracted from the GEO database, specifically focusing on human samples. Gene expression variance quantification was conducted utilizing the limma analytical toolkit, applying significance thresholds set at P < 0.05 alongside a minimum expression variation threshold of 1.5-fold. Additionally, single-cell transcriptomic data from obese asthmatic children were analyzed for cell annotation, interaction mapping, and pseudotime trajectory using R packages (Limma, Seurat, Dplyr, and Magrittr). In vitro experiments, including CCK-8 proliferation assays, cell migration, ROS oxidative stress measurements, and qRT-PCR, were conducted to assess Selenbp1's role in macrophage M1 polarization. Results: Differential gene expression analysis identified significant transcriptomic changes in obese asthmatic children, particularly elevated Selenbp1 expression, which was closely associated with macrophage M1 polarization. Single-cell sequencing analysis revealed specific cellular subpopulations and interactions, emphasizing Selenbp1's role in mediating exercise-induced effects. In vitro experiments confirmed Selenbp1's involvement in altering macrophage activity, highlighting its contribution to disease progression. Conclusion: Research findings reveal that exercise-regulated Selenbp1-mediated modulation of macrophage M1 polarization constitutes a key mechanism underlying pediatric obesity-associated asthma progression. These findings suggest novel molecular targets and provide insights into the therapeutic potential of exercise for treating obese asthmatic children.