Presenter Status
Fellow
Abstract Type
Clinical Research
Primary Mentor or Principal Investigator
Bridgette L. Jones, MD
Presentation Type
Poster
Start Date
19-5-2026 11:00 AM
End Date
19-5-2026 12:00 PM
Abstract Text
Background: Adverse childhood experiences (ACEs) are associated with increased asthma risk and outcomes as well as cytokine and gene expression changes relevant to asthma. However, ACE effects on immune cells at the single‑cell gene expression level, remain unclear.
Objectives/Goal: To investigate how high versus low ACE exposure influence immune cell makeup and differentially expressed genes (DEGs) in immune cells of children with uncontrolled, persistent allergic asthma
Methods/Design: We analyzed data and samples obtained from 19 children with uncontrolled persistent allergic asthma. Single cell RNA sequencing was performed on isolated peripheral blood mononuclear cells. Cell clusters were identified using Seurat v4.3, and cell types were annotated based on DICE reference profiles via SingleR (v2.4.1). ACE exposure was determined via scores obtained from responses to validated questionnaires: ACE for parents and Center for Youth Wellness (CYW) ACE-Q parent for child. High stress was defined as ≥ 4 ACEs and Low stress defined as < 4 ACEs. Cell proportions were compared using Wilcoxon rank-sum tests with significance set at p< 0.05. DEGs were identified using Wilcoxon rank-sum with Bonferroni false discovery rate correction. False Discovery Rate < 0.05 were considered significant.
Results: Participants mean age was 11.2 years, 53% female, 74% African American/Black, and over 30% endorsed as high ACE. After filtering, 184,577 cells sequenced across 10 lanes were analyzed. CD4+ naïve T cells were most abundant overall. NK cells increased in high ACE exposure, while naïve B cells, and CD4+ simulated naïve T cells were decreased in low ACE exposure (p< 0.05). Differential expression analysis revealed >6700 DEGs, including key immune regulators involved in transcription, inflammation, and stress‑response genes relevant to asthma pathophysiology (p< 0.0001). Notable DEGs in NK cells across all ACE measures includes FKBP5, GNLY, and RPS4Y1 (p< 0.0001).
Conclusions: ACEs may influence inflammatory cellular makeup and expression of key genes linked to asthma pathophysiology. Early life stress may drive immune dysregulation and downstream pathways relevant to asthma severity and treatment response. Further work is needed to validate these findings.
Impacts of Adverse Childhood Experiences on Single-Cell Gene Expression among Children with Uncontrolled Asthma
Background: Adverse childhood experiences (ACEs) are associated with increased asthma risk and outcomes as well as cytokine and gene expression changes relevant to asthma. However, ACE effects on immune cells at the single‑cell gene expression level, remain unclear.
Objectives/Goal: To investigate how high versus low ACE exposure influence immune cell makeup and differentially expressed genes (DEGs) in immune cells of children with uncontrolled, persistent allergic asthma
Methods/Design: We analyzed data and samples obtained from 19 children with uncontrolled persistent allergic asthma. Single cell RNA sequencing was performed on isolated peripheral blood mononuclear cells. Cell clusters were identified using Seurat v4.3, and cell types were annotated based on DICE reference profiles via SingleR (v2.4.1). ACE exposure was determined via scores obtained from responses to validated questionnaires: ACE for parents and Center for Youth Wellness (CYW) ACE-Q parent for child. High stress was defined as ≥ 4 ACEs and Low stress defined as < 4 ACEs. Cell proportions were compared using Wilcoxon rank-sum tests with significance set at p< 0.05. DEGs were identified using Wilcoxon rank-sum with Bonferroni false discovery rate correction. False Discovery Rate < 0.05 were considered significant.
Results: Participants mean age was 11.2 years, 53% female, 74% African American/Black, and over 30% endorsed as high ACE. After filtering, 184,577 cells sequenced across 10 lanes were analyzed. CD4+ naïve T cells were most abundant overall. NK cells increased in high ACE exposure, while naïve B cells, and CD4+ simulated naïve T cells were decreased in low ACE exposure (p< 0.05). Differential expression analysis revealed >6700 DEGs, including key immune regulators involved in transcription, inflammation, and stress‑response genes relevant to asthma pathophysiology (p< 0.0001). Notable DEGs in NK cells across all ACE measures includes FKBP5, GNLY, and RPS4Y1 (p< 0.0001).
Conclusions: ACEs may influence inflammatory cellular makeup and expression of key genes linked to asthma pathophysiology. Early life stress may drive immune dysregulation and downstream pathways relevant to asthma severity and treatment response. Further work is needed to validate these findings.
Comments
Poster Board Number: 25