Molecular pathology of allergic disease - II: Upper airway disease

Allergic upper airway diseases such as allergic rhinitis and chronic sinusi tis are an increasing problem. Although the pathogenesis remains elusive, a n individual's genetic predisposition as well as exposure to the allergen a re currently considered factors in their development. Clinical symptoms of sneezing, rhinorrhea, and congestion are primarily a consequence of granulo cyte release of chemical mediators such as histamine, prostanoids, and leuk otrienes as well as the infiltration of inflammatory cells, Observations su bsequent to allergen provocation are comparable to natural exposure and as such much of our understanding of allergic responses is derived from this m odel, A prominence of CD4(+) T cells and eosinophils, synthesis and release of T(H)2 cytokines, and the coordinate expression of chemokines and adhesi on molecules are all characteristic of the allergic response observed in rh initis and sinusitis. Corticosteroids and immunotherapy target these inflam matory processes and have been observed to successfully reduce and shift th e predominantly T(H)2 environment toward T(H)1 cytokine expression. As our understanding of the pathophysiologic features of allergic upper airway dis ease improves, as well as the relationship between their development and th at of lower airway disease, new strategies of diagnosis and treatment will allow for more effective modulation of the allergic process and associated morbidity.