Ross Summer, PhD
To learn more about Dr. Summer’s background and how to contact him,
see his profile.
The Summer lab is a basic science laboratory whose overarching goal is to develop novel treatments for patients with various lung disease including Acute Respiratory Distress Syndrome and Pulmonary Fibrosis.
An overview of active projects is summarized below. We invite those interested in more a detailed view of our work to review some of our most recent publications.
Current research efforts focus on three projects:
Project 1: Elucidate the mechanisms by which obesity promotes the development of ARDS.
Acute respiratory distress syndrome (ARDS) is a severe form of respiratory failure that has no effective treatment and causes death in approximately 1/3 of all patients. Obesity is now recognized as an important risk factor for the development of ARDS but the mechanisms mediating this association are unknown. Dr. Summer's laboratory employs genetic and diet-induced obesity models to further elucidate the mechanisms by which obesity promotes the development of acute lung injury in mice. The primary objective of these studies is to identify unique biological pathways that can be exploited for developing novel treatments for patients with ARDS.
Project 2: Elucidate the mechanisms by which chronic alcohol exposure promotes the development of inflammatory lung diseases.
Chronic alcohol abuse is a major public health problem and leads to increased morbidity and mortality. Alcohol’s injurious effects are observed in all tissues, but certain organs, such the liver, brain and lung appear to be particularly susceptible to its ill effects. In the lung, heavy alcohol intake promotes the onset, and enhances the severity of various inflammatory lung conditions such as bacterial pneumonia and ARDS. In recent work, Dr. Summer’s laboratory has discovered a novel mechanism by which chronic alcohol ingestion induces functional impairments in the lung’s immune system. His group showed that chronic alcohol induces a wide range of metabolic changes that act together to promote triglyceride and fatty acid accumulation in the lung. Further, they show that lipid accumulation mediates many of the suppressive effects of alcohol on immune cell function. Collectively, these observations have led his group to begin testing whether lipid lowering therapies might be effective for treating various alcohol-related inflammatory lung disorders.
Project 3: Determine how metabolic disturbances in the lung epithelium contribute to the pathogenesis of pulmonary fibrosis.
Pulmonary fibrosis refers to a group of conditions that cause scarring of the lung. These conditions have limited treatments, and those that are available are only marginally effective. It is now generally accepted that injury to the lung’s epithelium plays a causal role in the pathogenesis of pulmonary fibrosis but the mechanisms by which epithelial injury drives fibrotic responses remain unknown. Recent work in Dr. Summer’s laboratory indicates that metabolic disturbances in the lung epithelium play a pathogenic role in promoting fibrotic responses. These findings have led his laboratory to begin testing whether reversing these metabolic derangements might limit the onset or progression of lung fibrosis in mice.