Pathophysiology of bronchial inflammation: chemoreceptors as therapeutic targets.
Asthma is an inflammatory disease characterized by reversible airway obstruction from a combination of bronchoconstriction and inflammatory changes including airway edema, infiltration of inflammatory cells such as eosinophils, mast cells, CD4+ T helper cells and monocyte/macrophages. Pharmacotherapy approaches include relievers of acute symptoms and controllers of inflammation. Inhaled corticosteroids are the sentinel therapy for asthma inflammation but are not always totally effective for a variety of reasons. With the increased understanding about the molecular basis for asthma inflammation, new therapies are emerging to target specific molecular networks, including antibodies against IgE and the TH2 cytokine IL-5; soluble IL-4 receptors and recombinant TH1 cytokines such as IL-12. Further, allergen immunotherapy 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 of these modalities have their potential strengths and weaknesses, the approach offers a fresh attempt to better define the syndrome called asthma, show diversity of etiologies within even the same patient, and develop more effective, long lasting therapies for patients with this condition.
Marshall
G D
GD
Division of Allergy and Clinical Immunology, University of Texas-Houston Medical School, USA.
D000485:Allergens / Q000276:immunology; D001249:Asthma / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy; D002628:Chemoreceptor Cells / Q000502:physiology*; D016207:Cytokines / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D007167:Immunotherapy; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D000485:Allergens; D016207:Cytokines; D007073:Immunoglobulin E