Samir Kelada, PhD MPH

EMAIL: samir_kelada@med.unc.edu

PERSONAL WEBSITE: https://www.med.unc.edu/genetics/directory/samir-kelada-phd-mph/

PUBLICATIONS: Publications Link

Broadly speaking, my research interests lay in the arena of gene-environment interactions (GxE) in obstructive respiratory diseases. I view the identification and characterization of GxE as a means by which to understand population and individual-level disease susceptibility and a way to identify new disease mechanisms.

My lab’s research has addressed GxE in three primary contexts:
(1) with allergen exposure in mouse models of asthma, focusing particularly on the phenotypes of airway remodeling and concomitant mucus production
(2) with air pollutant exposure in development of inflammation and injury in models of asthma and COPD exacerbations
(3) with chronic air pollutant exposure and airway remodeling, to understand how air pollutants influence the development of asthma and COPD

The approaches I have used to identify GxE have evolved over time. I was originally trained in using epidemiologic (observational) approaches, then transitioned to using model systems in which we can control both G and E components to maximize power to detect GxE. This has primarily involved use of genetically diverse mouse genetic reference populations to map quantitative trait loci (QTL) for relevant phenotypes, and more recently we have begun to use human bronchial epithelial cells from tissue bank donors of diverse genetic ancestries. In both cases, we focus on the role of variants that alter gene expression at baseline (eQTL) or as a function of exposure (response eQTL), and couple these measurements with other responses (e.g. cytokine production) to identify gene regulatory models in which we can statistically infer variant to phenotype relationships, which are then experimentally validated to prove causality.