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Environmental toxins may cause body's defenses to worsen lung disease

he cell receives a signal that the tissue is infected, it will automatically destroy it to protect the body from disease.

"The immune system thinks it's eradicating disease from the body when it destroys cells that have been damaged by environmental toxins, but in chronic lung disease that destruction may be doing more harm than good," he says.

Chronic pulmonary diseases cause irreversible damage and inflammation in the lungs that lead to scarring and narrowing of the airways. The most common of these diseases are obstructive pulmonary disease, chronic bronchitis and emphysema. When a large amount of tissue is destroyed, Borchers says, it can cause irreparable damage to the elasticity of the lung and lead to additional health problems.

Using an animal model, Borchers will expose surface cells in the lung to two environmental toxins--the bacteria pseudomonas aeruginosa, a major cause of in-hospital infections, and acrolein, an air pollutant found in tobacco smoke, smog and diesel exhaust--to determine how cells respond to infection and toxicant-induced cell damage.

"By looking at how the cells react to these stimuli, we hope to gain insight into what triggers and mediates the immune system response," Borchers says.

This will help scientists determine which lymphocytes are important for regulating damage in the lungs, so they can develop ways to "tweak" the immune system and prevent the lymphocytes from causing additional damage to already-injured tissue.

Borchers says understanding these pathways could play an important role in future drug treatments for patients with chronic obstructive pulmonary disease and the basic scientific findings may also have applications in asthma and cystic fibrosis as well as other chronic lung diseases.

The overall goal of the study is to expand existing scientific knowledge of how epithelial cells in the lungs communicate with the immune system in response to environmental an
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Source:University of Cincinnati


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