Australian researchers have demonstrated that blocking granulocyte macrophage-colony stimulating factor (GM-CSF) can reduce or prevent cigarette smoke-induced lung inflammation in mice, according to findings published in the American Thoracic Society’s American Journal of Respiratory and Critical Care Medicine. Inflammation underlies the disease process of chronic obstructive pulmonary disease (COPD) and many other smoking-related ailments. Because cigarette-induced lung inflammation responds poorly to current anti-inflammatory treatments, researchers have been focused on identifying more effective therapies.
Cigarette smoke triggers the release of GM-CSF and other cytokines and chemokines which cause activation and recruitment of more inflammatory cells into the lung, perpetuating the inflammatory response and exacerbating ongoing inflammation. Researchers have been interested in studying GM-CSF because it governs the growth, activation, and survival of leukocytes directly implicated in the pathogenesis of COPD.
The researchers exposed a group of mice, half of which had been treated with a GM-CSF blocking agent, anti-GM-CSF, and half of which were controls, to the equivalent of nine cigarettes of smoke each day for four days. At the end of the four days, the mice were killed and their lung tissue examined for the presences of inflammatory cells.
“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,” said Ross Vlahos, PhD, lead researcher on the study and senior research fellow with the lung disease research group at the University of Melbourne.