From Our 2010 Archives

Blocking Protein May Stem COPD

THURSDAY, March 18 (HealthDay News) -- Blocking a specific protein reduced or prevented smoking-related lung inflammation in mice, Australian researchers report.

Inflammation is associated with chronic pulmonary obstructive disease (COPD) and many other health problems caused by smoking.

In the study, researchers from the University of Melbourne focused on a protein called granulocyte macrophage-colony stimulating factor (GM-CSF), which controls the growth, activation and survival of leukocytes, the white blood cells that are part of the immune system and that play a role in the development of COPD.

The researchers exposed mice to the equivalent of smoke from nine cigarettes a day for four days. Half the mice were treated with a GM-CSF blocking agent (anti-GM-CSF). After four days, the rodents' lung tissue was examined for the presence of inflammatory cells.

"We found that anti-GM-CSF strongly reduced the number of potentially harmful white blood cells that infiltrate the lung after smoke exposure, as well as inhibiting the pro-inflammatory cytokine tumor necrosis factor (TNF)-a, the chemokine macrophage inflammatory protein-2 (MIP-2), which coordinates the movement of white blood cells into the lung," the study's lead researcher, Ross Vlahos, a senior research fellow with the lung disease research group at the University of Melbourne, said in a news release from the American Thoracic Society. "It also inhibited the protease MMP-12, which is known as one of the main enzymes able to destroy lung tissue."

"Cigarette smoke-exposed mice that were treated with an anti-GM-CSF had significantly less lung inflammation in comparison to untreated mice," Vlahos said. "This indicates that GM-CSF is a key mediator in smoke-induced lung inflammation, and its neutralization may have therapeutic implications in diseases such as COPD."

The findings could lead to new ways to fight COPD and other smoking-related diseases, the researchers indicated.

The study was published online recently in the American Journal of Respiratory and Critical Care Medicine.

-- Robert Preidt

Copyright © 2010 HealthDay. All rights reserved.

SOURCE: American Thoracic Society, news release, March 18, 2010





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