title: Targeting eosinophil biology in asthma therapy.
abstract: Due to their role as main effector cells in immune reactions against invading parasites, eosinophils have a plethora of molecules available to destroy these complex pathogens. Their role in allergic diseases such as bronchial asthma, where they do not have to conquer pathogens, is discussed controversially. However, since eosinophils were identified by Paul Ehrlich in tissue and sputum of patients with asthma, it was regarded that their important defensive role turns into its direct opposite so that these cells cause destruction of the airway tissue, ultimately leading to the formation of disease phenotype. Thus, eosinophils were identified as a prime target in therapeutic intervention of bronchial asthma. Over the last years, a number of mediators and receptors involved in the regulation of eosinophil recruitment, chemotaxis, activation, survival, and apoptosis have been identified. Some of these molecules have been addressed in vitro and in animal models of experimental asthma to evaluate their therapeutic potential in asthma. A few of these candidates have been tested in clinical studies, which produced surprising results questioning the role of eosinophils in asthma pathogenesis. This article summarizes these approaches and gives a critical overview about further candidate molecules that have been recently discussed as targets for an eosinophil-specific asthma therapy.
authors.affiliation: Experimental Pneumology, Research Center Borstel, Parkallee 1, D-23845 Borstel, Germany 1887402. mwegmann@fz-borstel.de
authors.forename: Michael
authors.initials: M
authors.lastname: Wegmann
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology; D004804:Eosinophils / Q000187:drug effects* / Q000276:immunology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D010641:Phenotype; D054397:Receptors, CCR3 / Q000187:drug effects / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D018927:Anti-Asthmatic Agents; D018836:Inflammation Mediators; D054397:Receptors, CCR3; D043562:Receptors, G-Protein-Coupled