Beata Kosmider, PhD

Research Interests

Two million Americans suffer from chronic obstructive pulmonary disease, contributing to 100,000 deaths every year. Cigarette smoke induces oxidative stress and is the most common risk factor of lung injury and pulmonary emphysema. Emphysema is caused by the destruction of alveolar wall septa. Therapy against this disease is limited. My translational research interests are centered on lung injury in emphysema. Particularly, we have focused on human primary alveolar type II cell injury. These cells make and secrete pulmonary surfactant. They proliferate to restore the epithelium after damage to the more sensitive alveolar type I cells. We isolate human primary alveolar type II cells to study the mechanism of the impairment of the antioxidant defense system and repair induced by exposure to cigarette smoke. We also analyze inflammatory response and oxidative stress in these cells. Our research is focused on the enhancement of the antioxidant defense system to provide protection against oxidative stress-induced cell injury. We isolate murine alveolar type II cells to complement our study in humans. We use biochemistry, molecular, and cellular biology approaches to address our questions regarding cell injury by cigarette smoke and emphysema development. Understanding the mechanisms of this disease progression may lead to novel therapeutic strategies to slow down alveolar wall destruction.

Educational Background

• Postdoctoral Fellowship, Webb-Waring Institute for Cancer, Aging and Antioxidant Research, University of Colorado at Denver, Denver, CO
• Postdoctoral Fellowship, Texas A&M University System Health Science Center, Houston, TX
• PhD, Biology, University of Lodz, Poland
• MS, Physiology-Genetics, University of Lodz, Poland
• MS, Environmental Biology, University of Lodz, Poland

Memberships

• American Heart Association
• American Thoracic Society
• American Physiological Society

PubMed Publications

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