Cells and mediators in diisocyanate-induced occupational asthma

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Purpose of review

Diisocyanates are the most common cause of occupational asthma in many industrialized countries, and various pathogenic mechanisms have been suggested to be involved. Occupational asthma causes airway remodeling unless diagnosed and treated within a proper time frame. However, treatment modalities are limited because of an insufficient understanding regarding underlying pathogenic mechanisms.

Recent findings

Several immunological and nonimmunological mechanisms have been suggested, indicating that the pathogenesis of occupational asthma may be more complex than other types of asthma. Airway epithelial cells are the first to encounter diisocyanates and orchestrate various responses, such as cytokine release, oxidative stress generation, and autoantibody formation. Some evidence supports the involvement of adaptive immune responses. Additional evidence suggests that other mechanisms are involved in diisocyanate-induced occupational asthma. One such candidate mechanism is oxidative stress. Oxidative stress has been shown to trigger and aid in the development of diisocyanate-induced occupational asthma in human samples and genetic studies, and some therapeutic trials were performed based on this finding.


Diisocyanate-induced occupational asthma may be caused by a complex interaction of innate and adaptive immune responses. The knowledge presented in this review may help lead to the development of new treatment modalities through an increased understanding of occupational asthma pathogenesis.

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