title: Release of granule proteins from human eosinophils stimulated with mast-cell mediators.
abstract: BACKGROUND
  It has been suggested that mast cells and eosinophils are major effector cells in the pathogenesis of allergic diseases. However, the interaction of these cells has not been thoroughly elucidated. We examined eosinophil cationic protein (ECP) release and cytosolic free calcium concentration ([Ca2+]i) in human eosinophils induced by the major mast-cell mediators including cytokines.
  
  
  METHODS
  Eosinophils from healthy donors were stimulated with the major mast-cell mediators for 20 min after preincubation with cytochalasin B for 10 min. ECP in supernatants was measured by radioimmunoassay. Moreover, to examine changes of [Ca2+]i in eosinophils, Fura-2-loaded eosinophils were monitored for fluorescence changes after stimulus addition.
  
  
  RESULTS
  Of the tested mediators (prostaglandin [PG]D2, leukotriene (LT)B4, platelet-activating factor (PAF), histamine, LTC4, and eosinophil chemotactic factor of anaphylaxis [ECF-A]), LTB4 and PAF induced ECP release from eosinophils. Any cytokines produced by human mast cells, i.e., interleukin (IL)-4, IL-5, IL-8, tumor necrosis factor (TNF), or granulocyte-macrophage colony-stimulating factor (GM-CSF), did not induce ECP release in our system. ECP release triggered with LTB4 and PAF occurred at concentrations of 10(-8)-10(-6) M concentration-dependently. LTB4 and PAF also elicited a rise in [Ca2+]i in eosinophils. Neither PGD2, histamine, nor LTC4 induced ECP release, although they increased cytosolic calcium in eosinophils.
  
  
  CONCLUSIONS
  Of mast-cell mediators, LTB4 and PAF induced eosinophil degranulation. The contribution of LTB4 and PAF from mast cells to eosinophil degranulation may be important in the pathogenesis of allergic inflammatory diseases.
authors.affiliation: Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Takafuji
authors.forename: K
authors.initials: K
authors.lastname: Tadokoro
authors.forename: K
authors.initials: K
authors.lastname: Ito
authors.forename: T
authors.initials: T
authors.lastname: Nakagawa
mesh_terms: D001798:Blood Proteins / Q000187:drug effects* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002631:Chemotactic Factors, Eosinophil / Q000494:pharmacology; D016207:Cytokines / Q000494:pharmacology; D003600:Cytosol / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D015232:Dinoprostone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000187:drug effects* / Q000378:metabolism; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology*; D007700:Kinetics; D007975:Leukotriene B4 / Q000494:pharmacology; D017997:Leukotriene C4 / Q000494:pharmacology; D008407:Mast Cells / Q000378:metabolism; D010972:Platelet Activating Factor / Q000494:pharmacology; D015230:Prostaglandin D2 / Q000494:pharmacology; D012260:Ribonucleases
chemical_list: D001798:Blood Proteins; D002631:Chemotactic Factors, Eosinophil; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D010972:Platelet Activating Factor; D007975:Leukotriene B4; D017997:Leukotriene C4; D006632:Histamine; D012260:Ribonucleases; D015232:Dinoprostone; D015230:Prostaglandin D2; D002118:Calcium