title: Eosinophil-adhesion-inducing activity produced by antigen-stimulated mononuclear cells involves GM-CSF.
abstract: BACKGROUND
  The initial step of eosinophil accumulation in allergic inflammation is adhesion of circulating eosinophils to vascular endothelial cells (EC). There is evidence that the adhesive property of circulating eosinophils is upregulated following antigen exposure. Although the exact mechanism remains to be established, cytokine(s) produced by antigen-stimulated mononuclear cells is (are) likely key factor(s).
  
  
  OBJECTIVE
  The objective of this study was to examine the factor(s) responsible for eosinophil adhesion and migration induced by the antigen-stimulated mononuclear cells obtained from atopic asthmatics.
  
  
  METHODS
  Peripheral blood mononuclear cells (PBMC) isolated from house-dust-mite-sensitive bronchial asthmatics were cultured for 96 h in the presence or absence of 1 microg/ml Dermatophagoides farinae (Df) antigen. Eosinophils were isolated from peripheral blood of healthy subjects. Eosinophil-adhesion-inducing activity in the culture supernatants of PBMC was examined by the ability to modify the adhesion of eosinophils to human pulmonary microvascular endothelial cells (HPMEC) in the presence or absence of anti-cytokine/chemokine antibodies. Eosinophil migration induced by the supernatants was also examined.
  
  
  RESULTS
  Eosinophil adhesion to HPMEC was significantly augmented by the supernatants of Df-stimulated PBMC, which was significantly inhibited by anti-GM-CSF, but not by anti-IL-5, anti-RANTES, or isotype-matched controls. On the other hand, eosinophil migration induced by the supernatants was inhibited by anti-GM-CSF and partly by anti-RANTES.
  
  
  CONCLUSIONS
  Both eosinophil adhesion and migration induced by the antigen-stimulated PBMC involve GM-CSF. In contrast, RANTES is involved only in the eosinophil migration. These molecules may participate in the development of eosinophil accumulation at the allergic inflammation sites.
authors.affiliation: Pulmonary Division, Second Department of Internal Medicine, Saitama Medical School, Saitama, Japan. favre4mn@saitama-med.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Nagata
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Tabe
authors.forename: Y
authors.initials: Y
authors.lastname: Sakamoto
authors.forename: H
authors.initials: H
authors.lastname: Matsuo
mesh_terms: D000941:Antigens / Q000276:immunology*; D001249:Asthma / Q000097:blood; D002448:Cell Adhesion; D002465:Cell Movement; D018946:Chemokine CCL5 / Q000502:physiology; D004804:Eosinophils / Q000502:physiology*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000502:physiology*; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000502:physiology*
chemical_list: D000941:Antigens; D018946:Chemokine CCL5; D016178:Granulocyte-Macrophage Colony-Stimulating Factor