Illuminating Disease Pathways in Emphysema

Biomedical research at the Center for Inflammation, Translational and Clinical Lung Research at Temple University is increasing our understanding of complex diseases such as emphysema. Beata Kosmider, MS, PhD, is currently conducting NIH-funded research into the links between emphysema development and human primary alveolar type II (ATII) cell injury induced by oxidative stress. Emphysema, a subcategory of COPD with limited therapeutic options, consists of a unique pattern of alveolar wall destruction and airspace enlargement caused by damage to the alveolar-capillary (epithelial and endothelial) cells from cigarette smoke or other factors. ATII cells make and secrete pulmonary surfactant, and they proliferate to restore the epithelium after damage to the more sensitive alveolar type I cells.

Human lung used to isolate ATII cells and other cell types.

Dr. Kosmider and her colleagues determine ATII cell morphology, physiology and metabolism. Cells are isolated from discarded tissue obtained from patients with emphysema who had lung transplants and from organ donors without emphysema whose lungs were donated for medical research. Researchers also perform preclinical studies to define ATII cells’ role in innate immunity and the repair process after lung injury. Various cell types obtained from the same subject are used for a co-culture and analysis of cellular response to drug treatment.

Researchers in Dr. Kosmider’s laboratory have processed 394 human lungs obtained from the Temple Biobank and other sources. They isolate ATII cells and other cell types from lung tissue. Their work has demonstrated that oxidative stress due to environmental factors such as influenza virus and ozone induces ATII cell injury, which may make it harder for the lung to repair itself. They also study the mechanisms by which cigarette smoke may influence emphysema development, as well as potential therapeutic treatments to prevent ATII cell injury and lung disease progression.