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Involvement of prostanoids in cigarette smoking-induced pathophysiological effects in the lung.

Cigarette smoking is the major cause of chronic airway diseases (e.g. emphysema, chronic bronchitis, etc), which lead to morbidity and mortality in millions of smokers. Although the etiology of these smoking-related airway diseases is not completely understood, there is little doubt that chronic airway inflammation induced by cigarette smoke inhalation plays a critical part in causing the progressive pathological changes in lung structures and functions. Among the various inflammatory mediators endogenously released in the airways and lungs, increasing evidence has revealed the involvement of prostanoids in producing both acute and chronic pathophysiological effects of cigarette smoke on the respiratory tract. In this review, we have attempted to focus specifically on recent findings of elevated bioactivity of these autocoids caused by cigarette smoke inhalation and the resulting alteration of physiological functions of various target cells in the airways.