Samir Kelada
University of North Carolina at Chapel Hill, NC·Genetics
Ozone, a common outdoor air pollutant, inflames the airways and is linked to asthma and chronic obstructive pulmonary disease (COPD), a long-term lung disease that blocks airflow. People respond to ozone very differently, which suggests genes shape their risk.
- Fields
Genetics
Public Health & Epidemiology
Physiology
- Topics
ozone
air pollution
gene-environment interaction
- Grants
- 3 known grants, through Oct 2029
What they work on
- Determine whether Angpt1 or Rspo2 is the causal gene at a mouse chromosome 15 locus controlling ozone-induced airway injury, using knockdown, knockout and rescue experiments, and test the nearby human variant rs10086579 in three human cohorts.
- Map new gene-by-ozone interaction loci for acute and chronic ozone response in Collaborative Cross and Diversity Outbred mice, using gene expression mapping in alveolar macrophages, then test matching variants in the MESA-Air and Children's Health Study cohorts.
- Compare the gene activity and epigenomes of alveolar macrophages from mouse strains that adapt or fail to adapt to repeated ozone, and validate candidate regulators in vivo with lentivirus-based gene targeting.
- Test whether failure to adapt to ozone predicts chronic lung disease after 5-week exposure in Collaborative Cross mice, and whether altering macrophage gene expression changes the outcome.
- Map DNA variants that control gene expression and chromatin accessibility in ozone-exposed human bronchial epithelial cells from 300 donors, using RNA-seq, single-cell RNA-seq and ATAC-seq.
- Validate candidate genes and regulatory variants by knocking down genes in airway cells and testing variant links to ozone-induced neutrophil recruitment in 191 exposed volunteers.
More about the research
Finding gene-by-environment interactions (GxE), cases where a gene variant changes the effect of an exposure, is hard in human studies alone. The three projects combine genetically diverse mice, human airway cells and human cohorts to find which genes make some people vulnerable to ozone and how.
Why it matters
Ozone pollution contributes to asthma, COPD and other lung and heart illness worldwide. Finding the genes and pathways that make some people more vulnerable could help identify susceptible individuals, such as children at risk of asthma or adults at risk of COPD. It could also point to new prevention and treatment approaches for air pollution-induced lung disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Genetic mechanisms underlying maladaptive respiratory responses to air pollution
NIH · Jan 2025 – Oct 2029
Discovery of Gene-by-Air Pollution Interactions in Respiratory Disease using Genetically Diverse Mice with Validation in Humans
NIH · Sep 2025 – Sep 2029
Regulatory Genomics of Ozone Air Pollution Response in Vitro and In Vivo
NIH · Apr 2022 – Feb 2027
Closest labs
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University of Chicago, IL·Microbiology & Immunology
Define the immune cell landscape in blood from Amish and Hutterite children using single-cell RNA sequencing, comparing cell type proportions and gene activity between the low-asthma and high-asthma farming populations.
Stephanie Lovinsky-Desir
Columbia University, NY·Medicine & Clinical Research
Establish how dysanapsis, a mismatch between airway size and lung size, measured early in life relates to lung function trajectories through childhood and to dysanapsis at late adolescence, using 8 birth cohorts, spirometry and lung MRI.
Camron Bryant
Northeastern University, MA·Genetics
Sequence the whole genomes of SHR/NCrl and SHR/NHsd rat substrains and map behavioral QTLs for impulsivity, compulsivity, and cocaine self-administration traits in an F2 reduced complexity cross.
The school
University of North Carolina at Chapel Hill: 72 labs on PI Pages, $1.6B a year on research, 523 research doctorates a year.
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