title: [Comparison of the inhibitory effects of glucocorticoids on the expression of eotaxin in airway epithelial cell line BEAS-2B].
abstract: OBJECTIVE
  Inhaled corticosteroids play a pivotal role in the treatment of asthma. To observe the mechanisms of glucocorticoids, we focused our study on the comparison of several glucocorticoids' effects on eotaxin expression in the airway epithelial cells.
  
  
  METHODS
  Airway epithelial cell line BEAS-2B was cultured in vitro. Cells were preincubated with or without glucocorticoids (becromethasone dipropionate; BDP, budesonide; BUD, fluticasone propionate; FP) and stimulated with TNFalpha and/or IL-4. Protein levels of eotaxin in the supernatants of the cultured cells were determined by ELISA.
  
  
  CONCLUSIONS
  TNFalpha and IL-4 increased the levels of eotaxin in BEAS-2B cells. Combination of these cytokines synergistically upregulated the eotaxin expression as reported previously. Each glucocorticoid significantly inhibited the expression of eotaxin protein induced with TNFalpha and IL-4 and the compared efficacy was in order of FP>BUD>BDP. FP seemed most potent and the inhibitory effect was also observed with relatively low concentration such as 10 (-10)M. Taken together, the comparison of the potency of each glucocorticoid using airway epithelial cells may reflect the efficacy of these drugs in asthmatics.
authors.affiliation: First Department of Internal Medicine, Showa University School of Medicine, Japan.
authors.forename: Koushi
authors.initials: K
authors.lastname: Ieki
authors.forename: Satoshi
authors.initials: S
authors.lastname: Matsukura
authors.forename: Fumio
authors.initials: F
authors.lastname: Kokubu
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Kurokawa
authors.forename: Mio
authors.initials: M
authors.lastname: Kawaguchi
authors.forename: Hideki
authors.initials: H
authors.lastname: Kuga
authors.forename: Shin
authors.initials: S
authors.lastname: Watanabe
authors.forename: Shintaro
authors.initials: S
authors.lastname: Suzuki
authors.forename: Miho
authors.initials: M
authors.lastname: Odaka
authors.forename: Hiroko
authors.initials: H
authors.lastname: Takeuchi
authors.forename: Robert P
authors.initials: RP
authors.lastname: Schleimer
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Adachi
mesh_terms: D001249:Asthma / Q000378:metabolism / Q000473:pathology; D001980:Bronchi / Q000166:cytology*; D002460:Cell Line; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000096:biosynthesis*; D004847:Epithelial Cells / Q000378:metabolism*; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D015847:Interleukin-4 / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D005938:Glucocorticoids; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4