New mediator of smoking recruits

Freiburg, Germany — Current research suggests that smoking increases the production of osteopontin in the lungs, which contributes to the development of smoking-related lung disease. The related report by Prasse et al, “Essential role of osteopontin in smoking-related interstitial lung diseases,” appears in the May 2009 issue of The American Journal of Pathology.

Nearly one billion people worldwide smoke tobacco products. Long-term exposure to compounds found in smoke can lead to both cardiovascular and lung disease. Although lung exposure to cigarette smoke leads to immune cell recruitment and tissue fibrosis, how cigarette smoke causes these changes is largely unknown.

To determine if osteopontin, a molecule that attracts immune cells, mediates cell recruitment in smokers, Prasse et al compared osteopontin levels from smokers with different types of lung diseases, healthy smokers, and healthy non-smokers. They found high levels of osteopontin expression in patients with interstitial lung disease, whereas healthy smokers had lower levels, and healthy non-smokers produced no osteopontin. Osteopontin expression could be stimulated directly by nicotine treatment. In addition, expressing osteopontin in rat lung resulted in recruitment of immune cells, resulting in symptoms similar to smoking-related interstitial lung diseases. These results indicate that osteopontin may be pathogenic in smoking-initiated lung disease.

The article from Prasse et al “suggest[s] that chronic nicotine stimulation induced by cigarette smoking promotes macrophage and Langerhans cell accumulation in the lung via an increase in [osteopontin production].” Osteopontin and cellular receptors for nicotine may therefore be new targets for treating smoking related lung disease.

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