title: Topical steroids do not downregulate expression of growth-related oncogene-alpha in nasal polyps.
abstract: CONCLUSIONS
  Topical steroids did not affect expression of growth-related oncogene-alpha (GRO-alpha) in nasal polyps. The results of this study suggest roles for steroid-resistant gene expression in the pathogenesis of nasal polyps and point to the need for additional pharmacological strategies.
  
  
  OBJECTIVE
  Infiltration of inflammatory cells is believed to play a role in the development of nasal polyps. GRO-alpha is a chemokine that recruits and activates neutrophils and also possesses growth stimulatory and angiogenetic properties. An increased presence of GRO-alpha has been demonstrated in nasal polyps compared with normal nasal tissue. In this study we evaluate the presence and expression levels of GRO-alpha in nasal polyps before and after glucocorticoid treatment.
  
  
  METHODS
  Nasal polyps were surgically removed in patients before and 6 weeks after treatment with topically applied fluticasone. GRO-alpha gene expression and the presence of GRO-alpha peptide were detected in polyp tissue by means of in situ hybridization, quantitative real-time reverse transcriptase polymerase chain reaction and immunohistochemistry.
  
  
  RESULTS
  Strong GRO-alpha gene expression and the presence of GRO-alpha peptide were seen in both the epithelium and stromal inflammatory cells of nasal polyps. No differences in gene expression levels in tissue homogenates were found when untreated polyp tissue was compared with polyps treated for 6 weeks with topically applied steroids.
authors.affiliation: Department of Otorhinolaryngology, Lund University, Malmö University Hospital, Malmö, Sweden. Lars-Olaf.Cardell@med.lu.se
authors.forename: Lars-Olaf
authors.initials: LO
authors.lastname: Cardell
authors.forename: Jesper
authors.initials: J
authors.lastname: Bogefors
authors.forename: Anders
authors.initials: A
authors.lastname: Bjartell
authors.forename: Mikael
authors.initials: M
authors.lastname: Adner
authors.forename: Rolf
authors.initials: R
authors.lastname: Uddman
authors.forename: Arne
authors.initials: A
authors.lastname: Egesten
mesh_terms: D000287:Administration, Topical; D000328:Adult; D000730:Androstadienes / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D054360:Chemokine CXCL1; D018925:Chemokines / Q000096:biosynthesis / Q000235:genetics; D019743:Chemokines, CXC / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D000068298:Fluticasone; D015870:Gene Expression / Q000187:drug effects / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000235:genetics / Q000378:metabolism*; D009857:Oncogenes / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000730:Androstadienes; D000893:Anti-Inflammatory Agents; C475829:CXCL1 protein, human; D054360:Chemokine CXCL1; D018925:Chemokines; D019743:Chemokines, CXC; D000068298:Fluticasone