A potential biochemical mechanism for ameliorating the damage to the lungs of cigarette smoking might be in the future.
Oviously quitting is the best approach but this might be useful in people genetically predisposed to emphysema.
ScienceDaily (Mar. 18, 2010) — Researchers in Australia have demonstrated that blocking a certain protein can reduce or prevent cigarette smoke-induced lung inflammation in mice. Inflammation underlies the disease process of chronic obstructive pulmonary disease (COPD) and many other smoking-related ailments.
Cigarette smoking causes lung inflammation, which can lead to oxidative stress, emphysema, small airway fibrosis, mucus hypersecretion and progressive airflow limitation. Since the inflammatory reaction to cigarette smoke responds poorly to current anti-inflammatory treatments, there is intense research to identify more effective therapies for cigarette smoke-induce lung damage.
Granulocyte macrophage-colony stimulating factor (GM-CSF) is of special interest because it governs the growth, activation and survival of leukocytes directly implicated in the pathogenesis of COPD.
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,thereby perpetuating the inflammatory response and exacerbating ongoing inflammation. These activated and recruited inflammatory cells also release proteases such as matrix metalloproteinase (MMP)-12, which destroy the lung tissue, resulting in emphysema.
New Technique Reduces Tobacco Smoke Damage to Lungs in Mice