title: Suppressive effects of tranilast on eotaxin-1 production from cultured conjunctival fibroblasts.
abstract: OBJECTIVE
  Eotaxin, a CC-chemokine with selective chemotactic effects for eosinophils, has been reported to play an important role in allergic conjunctival diseases. We previously reported that eotaxin is produced by conjunctival fibroblasts and keratocytes on stimulation with Th2 cytokines. Tranilast is known to have anti-allergic properties. In this study, we examined the inhibitory effect of tranilast, an anti-allergic drug, on eotaxin-1 production from cultured conjunctival fibroblasts.
  
  
  METHODS
  Conjunctival fibroblasts obtained from normal patients were cultured in DMEM/F12 medium. On the fifth passage, the cells were transferred to a 96-well plate and, after starvation for 24 hr, TNF-alpha, IL-4, and tranilast or dexamethasone were added. After 48 hr, the concentrations of eotaxin-1 in the supernatants were measured by ELISA, and the cells were tested for eotaxin-1 expression by real-time PCR.
  
  
  RESULTS
  Eotaxin-1 production was observed on simultaneous stimulation with TNF-alpha and IL-4. This production was inhibited by both tranilast and dexamethasone. Inhibition of eotaxin-1 expression was also observed by real-time PCR.
  
  
  CONCLUSIONS
  Eotaxin-1 production from conjunctival fibroblasts was inhibited by both tranilast and dexamethasone. These results suggest that the anti-allergic effect of tranilast may be partly due to the inhibition of eotaxin-1 production from conjunctival fibroblasts.
authors.affiliation: Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
authors.forename: Richard Yudi
authors.initials: RY
authors.lastname: Hida
authors.forename: Yoji
authors.initials: Y
authors.lastname: Takano
authors.forename: Naoko
authors.initials: N
authors.lastname: Okada
authors.forename: Murat
authors.initials: M
authors.lastname: Dogru
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Satake
authors.forename: Kazumi
authors.initials: K
authors.lastname: Fukagawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Fujishima
mesh_terms: D018926:Anti-Allergic Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D054413:Chemokine CCL11 / Q000096:biosynthesis* / Q000235:genetics; D003228:Conjunctiva / Q000166:cytology*; D003907:Dexamethasone / Q000494:pharmacology; D004797:Enzyme-Linked Immunosorbent Assay; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D015847:Interleukin-4 / Q000494:pharmacology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D062367:ortho-Aminobenzoates / Q000494:pharmacology*
chemical_list: D018926:Anti-Allergic Agents; D054413:Chemokine CCL11; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D062367:ortho-Aminobenzoates; D015847:Interleukin-4; D003907:Dexamethasone; C012293:tranilast