Our group investigates the genetic and biological determinants of environmental and occupational lung disease. Our previous research has provided insight into the pathophysiology, biology, and genetics of environmental airway disease, pulmonary fibrosis, and innate immunity.
Our lab has identified a polymorphism—variation in the normal sequence of a gene—in TLR4, the receptor for endotoxin or lipopolysaccharide (LPS). This discovery is important because the polymorphism in TLR4 results in a blunted response to inhaled LPS, an enhanced risk of Gram-negative sepsis, and a decreased risk of atherogenesis in humans.
We have also recently discovered that epigenetic mechanisms may be contributing to the development of asthma, and have identified a major gene variant that predisposes individuals to develop pulmonary fibrosis. The group's current work focuses on identifying other genes that regulate the innate immune response, genes involved in the fibroproliferative response in the lung, epigenetic regulation of asthma, and gene-environment interactions in innate immunity, pulmonary fibrosis, and asthma. Our research in these areas has the potential to develop biomarkers for early identification of susceptible individuals, lead to novel concepts about the prevention and pathogenesis of these diseases, and to transform therapy in pulmonary fibrosis, microbial infections, sepsis and asthma.
Learn about active grant support for the Schwartz/Yang Lab.
Learn about the Children's Environmental Health Center (CEHC), whose goal is to investigate the etiology and pathogenesis of airway disease in children.
Learn about the Lung Genomics Research Consortium and the Familial Pulmonary Fibrosis research the Schwartz laboratory conducts.