title: RANTES production in nasal epithelial cells and endothelial cells.
abstract: BACKGROUND
  It is well documented that the chemokine that is regulated upon activation, normal T expressed and presumably secreted, RANTES, is produced by macrophages, platelets, fibroblasts, and renal tubular epithelial cells. Recently, however, production of RANTES by vascular endothelium and airway epithelial cells was demonstrated in human umbilical vein endothelial cells (HUVECs) and epithelial cell lines.
  
  
  OBJECTIVE
  This investigation was aimed at determining whether human nasal epithelial cells (HNECs) and human mucosal microvascular endothelial cells (HMMECs) produce RANTES when they are stimulated by several cytokines.
  
  
  METHODS
  HNECs and HMMECs were isolated from nasal mucosa and subsequent continuous subcultures and were stimulated either by IL-1 beta or by the combination of tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma).
  
  
  RESULTS
  After the combined stimulation by TNF-alpha and IFN-gamma, HNECs and HMMECs dramatically produced RANTES, as previously observed in HUVECs and bronchial epithelial cell line BEAS-2B. IL-1 beta also increased RANTES production to a lesser extent. We also demonstrated that the amount of RANTES induced by TNF-alpha and IFN-gamma was higher in HNECs and HMMECs obtained from patients with nasal allergy than in those from patients without allergy.
  
  
  CONCLUSIONS
  RANTES from HNECs and HMMECs likely plays a critical role in eosinophil infiltration of the nasal mucosa in subjects with nasal allergy.
authors.affiliation: Department of Otorhinolaryngology, Chiba University, School of Medicine, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Terada
authors.forename: K
authors.initials: K
authors.lastname: Maesako
authors.forename: N
authors.initials: N
authors.lastname: Hamano
authors.forename: T
authors.initials: T
authors.lastname: Ikeda
authors.forename: M
authors.initials: M
authors.lastname: Sai
authors.forename: T
authors.initials: T
authors.lastname: Yamashita
authors.forename: S
authors.initials: S
authors.lastname: Fukuda
authors.forename: A
authors.initials: A
authors.lastname: Konno
mesh_terms: D000293:Adolescent; D000328:Adult; D002478:Cells, Cultured; D018946:Chemokine CCL5 / Q000096:biosynthesis* / Q000235:genetics; D004357:Drug Synergism; D004730:Endothelium, Vascular / Q000378:metabolism*; D004848:Epithelium / Q000378:metabolism; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000166:cytology / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D018946:Chemokine CCL5; D007375:Interleukin-1; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma