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 mucosa l inflammation of mixed cellularity in addition to the characteristic airways hyperresponsiveness and reversible obstruction. Mast cell medi ators 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 p hase response is the abundant accumulation of eosinophils in the bronc hial respiratory mucosa that is enabled by profound effects of the Th2 cytokine, IL-5. Additionally the IL-4 gene cluster that is responsibl e for the levels of total serum IgE production has now been linked to asthma. With this new insight into the inflammatory mechanism; causing asthma, a mounting body of evidence exists to explain the recent incr eases in allergic disease prevalence resulting from environmental poll ution. Air pollution, including the contribution by diesel exhaust par ticle emissions, has been shown to enhance both nasal IgE production a nd the gene expression of Th2 cytokines. It is believed that diesel pa rticulates act as adjuvants in the immune system that promote the deve lopment of allergic inflammation.