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. 2010 Apr;136(4):335-9.
doi: 10.1001/archoto.2010.28.

Lipopolysaccharide induction of cyclooxygenase-2 in long-term nasal epithelial cultures in cystic fibrosis

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Lipopolysaccharide induction of cyclooxygenase-2 in long-term nasal epithelial cultures in cystic fibrosis

Ajnacska Rozsasi et al. Arch Otolaryngol Head Neck Surg. 2010 Apr.

Abstract

Objective: To evaluate the lipopolysaccharide induction of cyclooxygenase-2 (COX-2) in long-term epithelial cultures from nasal polyp tissue of patients with cystic fibrosis (CF) and severe nasal polyposis.

Design: Experimental and histologic study.

Setting: Department of Otorhinolaryngology, University of Ulm, Ulm, Germany.

Participants: Nasal polyp tissue was evaluated from 9 patients with CF and obstructing nasal polyps undergoing elective sinus surgery. Nasal mucosa from the hypertrophic inferior turbinate of 9 patients without a history of CF or aspirin intolerance undergoing nasal corrective surgery served as control specimens.

Interventions: Tissue culturing, Western blotting, and tissue staining with hematoxylin-eosin.

Main outcome measures: The expression and lipopolysaccharide induction of COX-2 was detected and compared with those of the control group. Tissue was analyzed for the presence of inflammatory cells such as neutrophils, eosinophils, mast cells, plasma cells, lymphocytes, and monocytes.

Results: COX-2 was detectable in tissue specimens from all of the patients with CF and control subjects. In patients with CF, however, COX-2 expression was significantly lower in lipopolysaccharide-stimulated, long-term cultured epithelial cells compared with control tissue. Polyps from patients with CF contained markedly more neutrophils, macrophages, and plasma cells than did nasal mucosa from hypertrophic inferior turbinates of controls.

Conclusions: COX-2 expression in lipopolysaccharide-stimulated, long-term cultured epithelial cells in patients with CF is decreased compared with that in hypertrophic turbinate mucosa. The estimated defect in lipopolysaccharide responsiveness and the reduced induction of COX-2 needs further investigation.

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