title: Eosinophils in asthma and other allergic diseases.
abstract: A hallmark of allergic disease is infiltration of the tissues with increased numbers of eosinophils. This is the result of the co-ordinated action of cytokines, particularly IL-5, CCR3 binding chemokines and the adhesion molecules P-selectin and VCAM-1, acting in concert to cause selective trafficking of eosinophils into allergic tissue. This process is orchestrated by the Th-2 allergen specific lymphocyte. While there is little data to support the view that eosinophils ameliorate the allergic process, although they could have an important role in the disordered repair that leads to permanently impaired function in some allergic diseases, the evidence that they cause many of the pathophysiological features of allergic disease, while strong, remains circumstantial. Much of the data could be interpreted just as easily to suggest that eosinophils are bystander cells; markers of a certain type of pathological process, but not impinging upon it. The most direct evidence for a pathological role rests on the toxicity of the eosinophil granule proteins for bronchial epithelium and the bronchoconstrictor actions of the sulphidopeptide leukotrienes. The actions of LT antagonists in asthma which are certainly beneficial, but in most cases are not as effective as glucocorticoids, could be interpreted both for and against the eosinophil. In this paper we have focused on the studies that ask most directly the question of whether eosinophils are important effector cells in the pathogenesis of allergic disease. We conclude with a qualified affirmative. Even if they are only bystander cells they remain clinically important as diagnostic markers and a guide to the management of allergic disease.
authors.affiliation: Division of Respiratory Medicine, Institute for Lung Health, University of Leicester School of Medical, Glenfield Hospital, Leicester, UK.
authors.forename: A J
authors.initials: AJ
authors.lastname: Wardlaw
authors.forename: C
authors.initials: C
authors.lastname: Brightling
authors.forename: R
authors.initials: R
authors.lastname: Green
authors.forename: G
authors.initials: G
authors.lastname: Woltmann
authors.forename: I
authors.initials: I
authors.lastname: Pavord
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001249:Asthma / Q000276:immunology* / Q000628:therapy; D016535:Bronchial Hyperreactivity; D016207:Cytokines / Q000276:immunology*; D004804:Eosinophils / Q000502:physiology*; D006373:Helminthiasis / Q000276:immunology; D006801:Humans; D015848:Interleukin-5 / Q000276:immunology; D008168:Lung / Q000276:immunology* / Q000503:physiopathology; D013183:Sputum / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D016207:Cytokines; D015848:Interleukin-5