Peer-reviewed article
Violence-Related Distress, Nasal Epithelial Gene Expression, and T17-High Asthma in Youth.
Yue M, Gaietto K, Xu Z, Han YY, Forno E et al. ·
Summary
Written by AI, not yet AICS's view · claude-haiku-4-5-20251001This study examined how violence-related distress affects asthma in youth aged 8-20 years by looking at changes in nasal gene expression. Researchers combined data from three cohorts of children with asthma, mostly from minority backgrounds in Puerto Rico and the United States. They found nine genes that were linked to both violence-related distress and a specific type of asthma (T17-high asthma). These genes are involved in immune and inflammatory responses, and understanding them could lead to new treatments for children experiencing both violence and asthma.
Key points
- Nine genes (S100A7A, CCL2, CCL8, CXCL9-11, COL15A1, CD300E, LILRB1) were upregulated and associated with both violence-related distress and T17-high asthma
- Study involved 403 youth with asthma aged 8-20 years across three cohorts
- Violence-related distress was measured using the Checklist of Children's Distress Symptoms (CCDS) scale over the previous 6 months
- Two gene families involved (CC Motif Chemokine Ligand and CXC Motif Chemokine Ligand families) are related to immune and inflammatory responses
- Findings predominantly from minoritized youth, highlighting health disparities
Limitations
This is a cross-sectional study, so it cannot establish causation between violence-related distress and changes in gene expression or asthma endotypes. The findings describe associations at one point in time and cannot determine whether violence exposure leads to these biological changes or vice versa.
Abstract
Background Little is known about the mechanisms underlying the link between violence-related distress and asthma, particularly for asthma endotypes. Methods Cross-sectional analysis of violence-related distress in the previous 6 months (assessed using the Checklist of Children's Distress Symptoms [CCDS] scale) and nasal epithelial gene expression in 3 studies of youth with asthma aged 8-20 years: Stress and Treatment Response in Puerto Rican and African American Children with Asthma (STAR, n = 128), Epigenetic Variation and Childhood Asthma in Puerto Ricans (EVA-PR, n = 228), and Vitamin D Kids Asthma (VDKA, n = 47). We then tested for the association between expression of CCDS-related genes and nasal epithelial transcriptomic profiles corresponding to T2-high and T17-high asthma endotypes. Results In a meta-analysis of the CCDS score in the three cohorts, we identified 12 differentially expressed genes (DEGs) with false discovery rate-adjusted p value (FDR-P) < 0.05 and the same direction of association as in the discovery cohort (EVA-PR) in at least one replication cohort. Of these 12 DEGs, 9 (S100A7A, CCL2, CCL8, CXCL9-11, COL15A1, CD300E, and LILRB1) were upregulated and significantly associated with T17-high asthma in a meta-analysis of the three cohorts. Two genes belong to the CC Motif Chemokine Ligand family (CCL2, CCL8) and 3 belong to the CXC Motif Chemokine Ligand family (CXCL9, CXCL10, and CXCL11). Conclusion Nine novel genes were associated with violence-related distress and T17-high asthma in three cohorts of predominantly minoritized youth with asthma. Our findings may help uncover biologic processes underlying the violence-asthma link and could represent novel therapeutic targets for T17-high asthma.
Findings the Hub has extracted
Each claim below is labelled by its type of design and links back to this report.
- Intervention
- Measurement and analysis of association between violence-related distress (via CCDS scale) and nasal epithelial gene expression profiles
- Population
- Youth aged 8-20 years with asthma (predominantly minoritized children from Puerto Rico and African American backgrounds); 403 total participants across three cohorts
Key finding
Nine genes significantly upregulated and associated with both violence-related distress and T17-high asthma across meta-analysis of three cohorts
M et al. · Europe PMC · 1 Feb 2026