The Klesney-Tait lab investigates the intersection of lung immunology, neutrophil biology, and triggering receptor expressed on myeloid cells 1 (TREM-1.) The lungs represent a unique challenge for the immune system given their immense surface area, continuous exposure to the environment, and intricate architecture. Neutrophils are the most abundant leukocyte in the body and are often considered as "first responders" to infection and inflammation. TREM-1 is a surface receptor that acts to amplify innate inflammatory signaling through other receptors such as Toll-like receptors. The role of TREM-1 is context-dependent. TREM-1 plays an important role in appropriate immune responses, but in highly inflammatory states such as sepsis TREM-1 exacerbates disease. Utilizing mouse models of airway hyper-reactivity, we are currently investigating the roles of neutrophils and TREM-1 in asthma. Previous work in the lab has demonstrated that TREM-1 deficient neutrophils have an impaired ability to migrate across lung epithelium and generate superoxide. Preliminary evidence suggests that TREM-1 deficient mice are resistant to developing airway hyperreactivity. Our investigations aim to better understand which effects of TREM-1 deficiency contribute to protection from airway hyperreactivity.