title: [Eosinophil activation by epithelial cells of the respiratory mucosa. Comparative study of normal mucosa and inflammatory mucosa].
abstract: BACKGROUND
  To investigate the effect of epithelial cells from respiratory mucosa on eosinophil activation.
  
  
  METHODS
  Epithelial cell cultures were obtained from healthy nasal mucosa and nasal polyps. Eosinophils were isolated from peripheral blood and incubated with epithelial cell conditioned media (HECM) in the presence or absence of dexamethasone (10 microM). Eosinophil survival, expression of EG2 and CD69, and production of eosinophil cationic protein (ECP) and leukotriene C4 (LTC4) were evaluated. Cytokine levels in HECM were assessed by ELISA.
  
  
  RESULTS
  HECM induced eosinophil survival (78.6 +/- 9.9% for nasal mucosa, and 92.6 +/- 15% for nasal polyps) compared to controls (1 +/- 0.8%; p < 0.05). Dexamethasone blocked HECM induced eosinophil survival, this effect being greater when eosinophils were primed with nasal mucosa HECM. HECM promoted EG2 expression in eosinophils (47.9 +/- 9.1% for nasal mucosa, and 58.5 +/- 11.8% for nasal polyp) compared to controls (8.1 +/- 3.7%; p < 0.01). HECM had no effect on both CD69 expression and LTC4 release but decreased ECP secretion. Levels of interleukin (IL)-8 (35,700 +/- 7,300 pg/ml), IL-1 beta (11.3 +/- 1.8 pg/ml) and TNF-alpha (38.2 +/- 11 pg/ml) on nasal polyps HECM were significantly higher than on nasal mucosa HECM (17,600 +/- 2,700, 5.4 +/- 0.7 and 16.8 +/- 1.4 pg/ml, respectively; p < 0.05).
  
  
  CONCLUSIONS
  Epithelial cells from respiratory mucosa proved to have potential to increase eosinophil survival and activation. The lower inhibitory effect of dexamethasone on nasal polyps induced eosinophil survival and activation may be caused by a higher release of eosinophil activating factors from nasal polyp epithelial cells (inflammed tissue) compared to nasal mucosa.
authors.affiliation: Hospital Clínic i Provincial, Departament de Medicina, Universitat de Barcelona.
authors.forename: J
authors.initials: J
authors.lastname: Mullol
authors.forename: A
authors.initials: A
authors.lastname: Xaubet
authors.forename: E
authors.initials: E
authors.lastname: López
authors.forename: J
authors.initials: J
authors.lastname: Roca-Ferrer
authors.forename: T
authors.initials: T
authors.lastname: Carrión
authors.forename: J
authors.initials: J
authors.lastname: Roselló-Catafau
authors.forename: C
authors.initials: C
authors.lastname: Picado
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis; D001798:Blood Proteins / Q000096:biosynthesis; D002470:Cell Survival; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000276:immunology*; D004847:Epithelial Cells; D004848:Epithelium / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology; D018836:Inflammation Mediators / Q000032:analysis; D037181:Lectins, C-Type; D017997:Leukotriene C4 / Q000096:biosynthesis; D009297:Nasal Mucosa / Q000166:cytology* / Q000276:immunology*; D012260:Ribonucleases; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D037181:Lectins, C-Type; D017997:Leukotriene C4; D012260:Ribonucleases; D000099192:CD69 Antigens