An update on the immunopathogenesis of asthma as an inflammatory disease enhanced by environmental pollutants.

The pathogenesis of asthma now centers on the role of bronchial mucosal inflammation of mixed cellularity in addition to the characteristic airways hyperresponsiveness and reversible obstruction. Mast cell mediators play an early role in the asthmatic airway response but through induced arachidonic acid metabolites and cytokine production may also participate in the late phase response. A unique feature of the late phase response is the abundant accumulation of eosinophils in the bronchial respiratory mucosa that is enabled by profound effects of the Th2 cytokine, IL-5. Additionally, the IL-4 gene cluster that is responsible for the levels of total serum IgE production has now been linked to asthma. With this new insight into the inflammatory mechanisms causing asthma, a mounting body of evidence exists to explain the recent increases in allergic disease prevalence resulting from environmental pollution. Air pollution, including the contribution by diesel exhaust particle emissions, has been shown to enhance both nasal IgE production and the gene expression of Th2 cytokines. It is believed that diesel particulates act as adjuvants in the immune system that promote the development of allergic inflammation.