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Lung Damage from Tobacco Smoke Reversed in Mouse Study

Kathleen Blanchard's picture

Researchers have found a new technique that blocks an inflammatory protein and reverses lung damage from tobacco smoke in a mouse study. The findings could lead to novel treatments for patients with COPD and smoking related lung diseases.

Granulocyte macrophage-colony stimulating factor (GM-CSF) is released from the effect of tobacco smoke and leads to lung inflammation, destroying the lung tissue and resulting in emphysema. Blocking GM-CSF reduced the inflammation and lung damage from tobacco smoke, reversing the harmful effect of tobacco smoke in mice given a GM-CSF blocking agent.

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Ross Vlahos, Ph.D., a senior research fellow with the lung disease research group at the University of Melbourne says, "Cigarette smoke-exposed mice that were treated with an anti-GM-CSF had significantly less lung inflammation in comparison to untreated mice. 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 researchers exposed mice to tobacco smoke - half were given the GM-CSF blocking agent and the other half were used as controls. After subjecting the mice to tobacco smoke that was equivalent to nine cigarettes daily for four days, researchers killed the mice then examined their lung tissue, finding that the GM-CSF blocking agent "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)" that could lead to lung cancer.

Quitting smoking is still the best way to prevent and reverse lung damage from tobacco smoke warns Dr. Vlahos. "Our treatment deals with cigarette smoke-induced lung inflammation involved in COPD, not cancer and other smoking-related ailments. Quitting remains the best and only cure for smoking-related lung disease." The findings that damage from tobacco smoke was reversed in mice by blocking GM-CSF could also have clinical applications for other inflammatory related disease.

American Journal of Respiratory and Critical Care Medicine