From Our 2010 Archives
Blocking Protein May Stem COPD
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THURSDAY, March 18 (HealthDay News) -- Blocking a specific protein reduced or prevented smoking-related lung inflammation in mice, Australian researchers report.
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
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SOURCE: American Thoracic Society, news release, March 18, 2010