Pathophysiology of bronchial inflammation: Chemoreceptors as therapeutic targets

Asthma is an inflammatory disease characterized by reversible airway obstru ction from a combination of bronchoconstriction and inflammatory changes in cluding air-way edema, infiltration of inflammatory cells such as eosinophi ls, mast cells, CD4+ T helper cells and monocyte/macrophages. Pharmacothera py approaches include relievers of acute symptoms and controllers of inflam mation. Inhaled corticosteroids are the sentinel therapy for asthma inflamm ation but are not always totally effective for a variety of reasons. With t he increased understanding about the molecular basis for asthma inflammatio n, new therapies are emerging to target specific molecular networks, includ ing antibodies against IgE and the TH2 cytokine IL-5; soluble IL-4 receptor s and recombinant TH1 cytokines such as IL-12. Further; allergen immunother apy for asthma is based upon its ability to change a TH2 to a TH1 response by inhibiting IL-4 and/or stimulating IFN gamma production. Although each o f these modalities have their potential strengths and weaknesses, the appro ach offers a fresh attempt to better define the syndrome called asthma, sho w diversity of etiologies within even the same patient, and develop more ef fective, long lasting therapies for patients with this condition.