We study maternal effects on the immune system and development of allergic diseases, with a particular focus on asthma. Maternal effects are defined as influences of maternal environment, genotype or phenotype on the phenotype of the offspring. Maternal effects have been observed in a number of species, including mice and humans, for several environmental factors and in several tissues and systems of the offspring, including their immune system. Maternal effects may be beneficial, increasing offspring adaptation to changes in the environment and preventing a disease, and harmful, leading to a disease. List of maternally-influenced diseases includes asthma. The existence of maternal effects in asthma has been hypothesized because 1) asthma frequently starts in the first years of life, 2) aberrant gene variants account for only a small proportion of asthma prevalence (GWAS and rare variant studies), 3) childhood asthma associates with maternal environmental exposures and health status. Harmful maternal exposures and phenotypes with positive associations with childhood asthma include road traffic-related air pollution, cigarette smoke and maternal stress. Maternal environmental factors with negative association with childhood asthma include certain microorganisms, and in particular, bacteria present in the farming environment. The overarching goal of our laboratory is to delineate mechanisms underlying maternal effects on asthma. More specific goals are to define maternal information that is transferred to offspring, or lost and not transmitted to offspring, elucidate routes of information transfer (placenta, breast milk, gametes), delineate offspring cells and pathways that are programmed by this information, and study how these cells and pathways contribute to the development of asthma. We have particular interest in cells and pathways of the immune system. The translational goals are to identify early-life biomarkers of predisposition to asthma in humans and define molecular targets for development of preventive drugs.
Magdalena Maria Gorska, MD, PhD
Projects & Methods
To begin addressing our goals, we developed a mouse model, inducing asthma susceptibility in young mice by exposing their mothers to diesel exhaust particles (DEPs). Learn More
Qian Q, Chowdhury BP, Sun Z, Lenberg J, Alam R, Vivier E, Gorska MM. Maternal diesel particle exposure promotes offspring asthma through NK cell-derived granzyme B. J Clin Invest. 2020, 130:4133-4151. PMID: 32407293; PMCID: PMC7410053.
Lenberg J, Qian Q, Sun Z, Alam R, Gorska MM. Pre-pregnancy exposure to diesel exhaust predisposes offspring to asthma through IL-1β and IL-17A. J Allergy Clin Immunol. 2018, 141:1118-1122.e3. PMCID: PMC5844783.
Manners S, Alam R, Schwartz DA, Gorska MM. A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust. J Allergy Clin Immunol. 2014, 134:63-72.e7. PMCID: PMC4065237.
We are thankful to National Institutes of Health, national organizations, institutions and private donors for their generous support of our research. Learn More
Job & Training Opportunities
We welcome motivated postdocs, graduate students and technicians to inquire about training opportunities in our lab.