title: [The roles of adhesion molecules, cytokines and chemokines in allergic inflammation].
abstract: Recently, adhesion molecules, as well as eosinophils, have been found to play an important role in the inflammatory processes in allergic disease. We demonstrated here as below. Characteristics of adhesion molecules expression on eosinophils in asthma, namely, high-intensity expression of adhesion molecules. Induction of adhesion molecule expression by PAF and RANTES and in addition induction by the supernatant of mononuclear cells from mite-allergic asthmatic patients stimulated with mite-allergen as well as with a combination of the recombinant IL-3, GM-CSF and IL-5. Elevated soluble ICAM-1 in bronchial asthma. Moreover, the presence of a large variety of membrane receptors and the identification of cytotoxic molecules (mainly granule basic proteins) have indicated that eosinophils should be considered as effector cells. We therefore investigated the possible release of granule proteins in response to signaling from ICAM-1 and its ligands. The concentrations of eosinophil cationic protein and eosinophil-derived neurotoxin in supernatants of eosinophils were significantly greater (p < 0.05) in the presence of recombinant soluble ICAM-1 than without it. These results suggest that signaling from ICAM-1 and its ligands might induce eosinophil activation and might be involved in degranulation of eosinophil granule proteins. In addition, reactive oxygen species generated by eosinophils have also been considered capable of causing airway injury at the inflamed focus. We examined the effect of recombinant soluble ICAM-1 and its ligands on eosinophil-induced radical oxygen products. Recombinant soluble ICAM-1 augmented eosinophil oxidative metabolism. It was concluded that signaling via adhesion molecules might play an important role in the pathogenesis of allergic inflammation through activation of eosinophils, such as through an increase in oxidative metabolism or degranulation of eosinophil granule proteins.
authors.affiliation: Department of Clinical and Laboratory Medicine, Akita University School of Medicine.
authors.forename: J
authors.initials: J
authors.lastname: Chihara
mesh_terms: D000818:Animals; D001249:Asthma / Q000097:blood; D015815:Cell Adhesion Molecules / Q000502:physiology*; D018946:Chemokine CCL5 / Q000502:physiology; D018925:Chemokines / Q000502:physiology*; D016207:Cytokines / Q000096:biosynthesis / Q000502:physiology*; D004804:Eosinophils / Q000502:physiology; D006801:Humans; D006967:Hypersensitivity / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D018946:Chemokine CCL5; D018925:Chemokines; D016207:Cytokines; D018799:Intercellular Adhesion Molecule-1