title: Impact of ozone exposure on prostaglandin release in nasal polyps.
abstract: A dysregulation of the cyclooxygenases and a leukotriene/prostaglandin imbalance are assumed to be part of the pathogenesis of the aspirin (ASA) intolerance syndrome. Ozone is an air pollutant with known proinflammatory effects on exposed epithelia, however, its impact on the expression of the cyclooxygenases 1 and 2 (cox1/2) and prostaglandin E(2) (PGE(2)) in the nasal mucosa is not well known. Therefore, we analyzed cox expression and PGE(2) levels after ozone exposure in nasal mucosa and in nasal polyps considering ASA intolerance. Isolated epithelial nasal cells from control subjects without chronic rhinosinusitis (CRS), and those from patients with nasal polyps with and without ASA intolerance were cultured and exposed in vitro to ozone. Cox1/2 expression levels were analyzed by immunohistochemistry and PGE(2) release by ELISA. After ozone exposure cox1/2 expression remained unchanged in all the three groups. PGE(2) release was lowered in cell cultures from controls and from polyps of ASA tolerant but not in those of ASA intolerant patients after ozone exposure. In the latter, PGE(2) expression remained unchanged. Our in vitro data suggest that aspirin tolerant patients with polyps might be more affected by ozone compared to aspirin intolerant ones. The potential clinical impact of impaired PGE(2) expression caused by ozone on the functions of respiratory epithelia remains to be clarified.
authors: Department of Otolaryngology, Head and Neck Surgery, University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, 55101 Mainz, Germany.
authors: Cheng Jing
authors: CJ
authors: Zhu
authors: Kai
authors: K
authors: Fruth
authors: Astrid
authors: A
authors: Schneider
authors: Wolf J
authors: WJ
authors: Mann
authors: Juergen
authors: J
authors: Brieger
mesh_terms: D000328:Adult; D000368:Aged; D000393:Air Pollutants / Q000009:adverse effects*; D015415:Biomarkers / Q000378:metabolism; D002470:Cell Survival; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D051545:Cyclooxygenase 1 / Q000096:biosynthesis / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000096:biosynthesis / Q000378:metabolism; D015232:Dinoprostone / Q000096:biosynthesis / Q000378:metabolism; D004724:Endoscopy; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D010083:Oxidants, Photochemical / Q000009:adverse effects; D010126:Ozone / Q000009:adverse effects*; D011453:Prostaglandins / Q000096:biosynthesis / Q000378:metabolism*; D020545:Respiratory Mucosa / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D012720:Severity of Illness Index; D014057:Tomography, X-Ray Computed; D055815:Young Adult
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D010083:Oxidants, Photochemical; D011453:Prostaglandins; D010126:Ozone; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D015232:Dinoprostone