The Lung Biology and Disease Program represents the coordinated efforts of more than 30 faculty members whose research focuses on the lung. The program members consist of both MD and Ph.D. faculty with research interests in basic science aspects of lung disease, translational and pre-clinical animal models, as well as clinical research.

Preclinical animal models: Cigarette-smoke induced acute and chronic lung injury (COPD model), hyperoxic lung injury, asthma, inhaled particle and gas-induced lung damage, infectious organisms including P. carinii, P. aeruginosa and Influenza, and ionizing radiation and chemotherapy induced lung damage. These models can be used to test a variety of compounds and biologics for efficacy. The program has expertise in Inflammation, Immunology, Toxicology, Pathology, Physiology and Clinical Translation.

Inhalation facilities: New state-of-the-art facilities are available for exposing animals to a variety of particles, gases and small molecules. This facility also has the capability of using gene therapeutic approaches for the treatment of lung diseases. The program also has a unique facility for exposing human beings to small molecules, gases, etc. via inhalation in one of the few purpose-built human inhalation chambers in the USA. Measurement of biomarkers in the blood, saliva and bronchoalveolar lavages (BAL) fluid is also accomplished.

Human tissues and samples: The group has ongoing efforts revolving around lung injury due to infection, trauma and toxicant induced-lung injury. These include access to human samples of lung tissue, BAL fluid, induced sputum etc from patient populations with COPD, asthma, lung injury of human lung fibroblasts from normal and diseased lung tissue. These cells are ideal for evaluating the effects of small molecules on human cells of biologic relevance.

Anti-inflammatory mediators: Investigation of certain novel small molecules developed here at Rochester that possesses anti-inflammatory activity. The approaches we have developed interfere with how cigarette smoke evokes an inflammatory response. Preliminary data in both mouse models of smoke-induced lung injury and testing on bona fide human lung structural cells have identified a novel pathway for regulating inflammation in the lung, and possibly other tissues.

Gene therapy for lung scarring: Investigators have developed gene therapeutic strategies to deliver molecules which inhibit key effectors such as transforming growth factor beta, cytokine crucial to the genesis of scarring in the lung, kidney, liver and skin. These diseases are currently untreatable, and are a leading cause of morbidity and mortality.