title: Expression of arachidonate metabolism enzymes and receptors in nasal polyps of aspirin-hypersensitive asthmatics.
abstract: BACKGROUND
  The pathogenesis of rhinosinusitis in aspirin-exacerbated airway disease is closely linked to the disequilibrium in arachidonic acid metabolism. Although considerable amounts of data concerning impaired eicosanoid production are available, the precise mechanism and pathogenesis of the disease are still unknown. The aim of the present study was to assess the expression of enzymes belonging to the arachidonic acid cascade and receptors for arachidonate derivative metabolites in nasal polyps from aspirin- hypersensitive (AH) and aspirin-tolerant (AT) patients with rhinosinusitis.
  
  
  METHODS
  Cells expressing cysteinyl leukotriene (CysLT) receptors (CysLT(1) and CysLT(2)), arachidonate 5-lipoxygenase, leukotriene B(4) receptor type 1, E-prostanoid receptors (EP(2) and EP(4)), cyclooxygenase (COX)-1 and COX-2 were detected by immunocytochemistry in nasal polyps obtained from 10 AH patients and 18 AT patients.
  
  
  RESULTS
  There was a significantly higher density of cells expressing CysLT(1) and CysLT(2) receptors in nasal polyps from AH patients than from AT patients (p < 0.001). In contrast, the density of cells expressing EP(2) receptor and COX-2 was significantly lower in AH patients than in AT patients (p < 0.02). The number of COX-2-positive epithelial cells was significantly reduced in AH polyps (p < 0.04).
  
  
  CONCLUSIONS
  The elevated number of nasal polyp cells expressing CysLT receptors and lack of cells expressing EP(2) receptor and COX-2 may be related to a more severe course of hyperplastic rhinosinusitis in aspirin hypersensitivity.
authors: Department of Allergology, Immunology and Dermatology, Medical University of Lodz, Lodz, Poland.
authors: Anna M
authors: AM
authors: Adamusiak
authors: Olga
authors: O
authors: Stasikowska-Kanicka
authors: Anna
authors: A
authors: Lewandowska-Polak
authors: Marian
authors: M
authors: Danilewicz
authors: Malgorzata
authors: M
authors: Wagrowska-Danilewicz
authors: Andrzej
authors: A
authors: Jankowski
authors: Marek L
authors: ML
authors: Kowalski
authors: Rafal
authors: R
authors: Pawliczak
mesh_terms: D000328:Adult; D000368:Aged; D016718:Arachidonic Acid / Q000378:metabolism*; D055963:Asthma, Aspirin-Induced / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D051545:Cyclooxygenase 1 / Q000235:genetics / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism*; D018450:Disease Progression; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000378:metabolism* / Q000473:pathology; D018077:Receptors, Leukotriene / Q000235:genetics / Q000378:metabolism*; D058306:Receptors, Prostaglandin E, EP1 Subtype / Q000235:genetics / Q000378:metabolism; D058307:Receptors, Prostaglandin E, EP2 Subtype / Q000235:genetics / Q000378:metabolism
chemical_list: D018077:Receptors, Leukotriene; D058306:Receptors, Prostaglandin E, EP1 Subtype; D058307:Receptors, Prostaglandin E, EP2 Subtype; D016718:Arachidonic Acid; C412375:cysteinyl leukotriene receptor 2; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C083169:leukotriene D4 receptor