Understanding how alveolar epithelial cells regenerate is crucial for developing new therapeutic strategies for emphysema. Cigarette smoke is the most common risk factor for developing this disease. Beata Kosmider, MS, PhD, at the Center for Inflammation and Lung Research has been awarded a U.S. Department of Defense (DoD) grant to study alveolar type II (ATII) cell injury and repair in emphysema. Dr. Gerard Criner and Dr. Karim Bahmed serve as co-investigators on this project.
Continuous cell replacement and repair are needed to maintain the alveolar epithelium (the barrier between inhaled air and the underlying lung tissue), especially after injury induced by exposure to harmful factors. ATII cells have stem cell potential; when needed, they proliferate and differentiate into alveolar type I (ATI) cells to restore a damaged alveolar surface so that it continues to permit efficient gas exchange. Therefore, ATII cell differentiation to ATI cells is of critical physiologic significance.
Extensive ATII cell apoptosis induced by exposure to cigarette smoke, and not compensated for by cell proliferation, impairs alveolar wall repair and contributes to the development of emphysema. We currently have a poor understanding of the mechanisms that drive ATII cell proliferation, resulting in a lack of strategies to enhance reepithelialization and prevent respiratory disease progression. With the DoD grant, Dr. Kosmider will study the repair of the damaged alveolar epithelium after injury induced by cigarette smoke and in emphysema. Identifying novel regulators of reepithelialization can suggest therapeutic strategies to stimulate lung regeneration in respiratory diseases. ■