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

The University of Cincinnati (UC) has received $2.4 million to study whether environmental toxicants can stimulate the body's natural defense system to cause additional damage in people with chronic lung diseases.

Michael Borchers, PhD, believes long-term exposure to certain environmental toxicants may activate a specific receptor--known as NKG2D--in lung cells that causes the immune system to attack stressed (damaged) lung tissue.

"When tissue is exposed to a pathogen (disease-causing agent), the immune system immediately wants to destroy the damaged cells so healthy tissue can take over," explains Borchers, assistant research professor of environment health at UC and principal investigator for the study.

"But when the lungs experience chronic, low-level damage, we believe at some point that damage exceeds the body's natural ability to repair tissue," he adds. "And through the destruction of lung tissue, it may actually start contributing to chronic lung disease instead of protecting against it."

UC scientists say when this happens repeatedly--such as through environmental tobacco or workplace exposures--it may cause the immune system to attack the damaged tissue in the same way it would if the tissue were infected with bacteria or a virus.

"The same signaling pathway necessary to protect the body from disease may actually have the opposite effect, causing harm in the lung when exacerbated by persistent exposure to environmental contaminants," Borchers explains.

By blocking the NKG2D receptor, Borchers believes he can stop the immune system response and minimize damage to delicate tissue in the lung.

Lymphocytes, the white blood cells responsible for targeting and fighting off infection in the body, continually survey the epithelial cells lining the lungs to identify and destroy diseased cells. If the lymphocyte recognizes the tissue, Borchers explains, it simply continues its survey for problems. But if t
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Source:University of Cincinnati


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