Novel Therapeutic Approaches for Allergic Rhinitis

Abstract

The last 2 decades have witnessed enormous changes in our understanding of allergic rhinitis. As we have begun to unravel the complex underlying immunologic and inflammatory pathophysiology of the disease, new therapeutic strategies as well as specific molecular and cellular constituents have emerged as potential targets for clinical intervention. These efforts also have shed light on the mechanisms by which current antiallergy medications act-or sometimes fail to be effe~tive.~, 31* 51*89 The similar pathophysiologic basis for allergic rhinitis and the often comorbid condition, asthma, was underscored in the recently published American Thoracic Society Workshop Summary on the Immunobiology of Asthma and Rhinitis: Pathogenic Factors and Therapeutic 0ptions.l8 In his conclusion, workshop chair, Thomas Casale,18 counsels readers to consider that ". . .allergic asthma and rhinitis represent a systemic disease affecting two organs, the lung and the nose. Asthma and allergic rhinitis share many of the same pathogenic factors, but they operate in different parts of the airway. Inflammatory cells and mediators are often the same, and there may be common alterations that occur in the immune system." Thus, therapeutic strategies and potential therapeutic agents found to be beneficial in the treatment of one airway target may show similar effects in the other. For this reason, and because many of the therapies now being developed are at early stages in their evolution,

The Role of Soluble Interleukin‐4 Receptor and Interleukin‐5 Antibody in Preventing Late‐Phase Allergy‐Induced Eustachian Tube Dysfunction

“…sIL-4R, which are almost the molecular equivalent of the extracellular domain of the cellular IL-4R, have been proposed recently to be a potential therapy for atopic disease. 15 Theoretically, by binding IL-4, these soluble receptors should inhibit binding with their cellular counterparts, thus reducing the allergic response (Fig 9A). Studies in both murine and human models have shown that this agent is effective in preventing the atopic response of inflammation and edema, as well as reducing the number and effectiveness of a number of molecular mediators of allergic disease.…”

“…sIL‐4R, which are almost the molecular equivalent of the extracellular domain of the cellular IL‐4R, have been proposed recently to be a potential therapy for atopic disease 15 . Theoretically, by binding IL‐4, these soluble receptors should inhibit binding with their cellular counterparts, thus reducing the allergic response (Fig 9A).…”