[Expression of adhesion molecules on eosinophils in relation to cytokines and chemotactic agents].
The functions of eosinophils in immunological reactions and their heterogeneity have recently generated a matter of great interest. Several characteristics of human eosinophil heterogeneity, as well as the existence of eosinophil subpopulations, called "normodense" and "hypodense", in diseases associated with hypereosinophilia, have been reported. Hypodense eosinophils can be distinguished by the increased expression of various membrane receptors including IL-5 receptor (J Exp Med 172: 1347) and various protein expression (J Immunol 142:4416). On the other hand, recently, adhesion molecules are considered to play an important role in inflammatory processes in allergic and immune reactions such as bronchial asthma. It was recently described that symptoms of bronchial asthma in animal model were in particular improved by means of anti-ICAM-1 (Intercellular adhesion molecule-1) monoclonal antibody (mAb). Thus, in thin study, we examined the characteristics of expression of adhesion molecules on human eosinophils obtained from hypereosinophilia (hypodense eosinophils). As results, high intensity expression of adhesion molecules (CR3, LFA-1 alpha, LFA-1 beta) on eosinophils obtained from patients with hypereosinophilia were observed. Furthermore, ICAM-1, which is ligand for LFA-1 molecules, was also expressed on eosinophils with hypereosinophilia. To extend our understanding of high intensity expression of adhesion molecules (CR3, LFA-1 alpha, LFA-1 beta, ICAM-1) on hypodense eosinophils, we examined whether chemotactic agents or eosinophilopoietic growth lymphokines (IL-3, GM-CSF, IL-5) is involved in adhesion molecule expression using an eosinophilic cell line named EoL-3. These characteristics of adhesion molecules on eosinophils were induced by some chemotactic agents and eosinophilopoietic growth lymphokines.(ABSTRACT TRUNCATED AT 250 WORDS)
Fourth Department of Internal Medicine, Kinki University School of Medicine.
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J
Chihara
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S
Nakajima
D000818:Animals; D001249:Asthma / Q000276:immunology / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000378:metabolism* / Q000502:physiology; D002450:Cell Communication; D016207:Cytokines / Q000378:metabolism / Q000502:physiology*; D004727:Endothelium / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D004802:Eosinophilia / Q000378:metabolism; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism*; D006801:Humans
D015815:Cell Adhesion Molecules; D016207:Cytokines