Low prostaglandin E2 and cyclooxygenase expression in nasal mucosa fibroblasts of aspirin-intolerant asthmatics

Autor: Roca-Ferrer, J., Pérez-Gonzalez, M., García-García, F. J., Pereda Cervera, Javier, Pujols, L., Alobid, Isam, Mullol i Miret, Joaquim, Picado, C.
Rok vydání: 2013
Předmět:
Zdroj: Roca-Ferrer J Pérez-Gonzalez M Garcia-Garcia FJ Pereda Cervera, Javier Pujols L Alobid, Isam Mullol, Joaquin Picado C. 2013 Low prostaglandin E2 and cyclooxygenase expression in nasal mucosa fibroblasts of aspirin-intolerant asthmatics. Respirology 18 4 711 717
RODERIC. Repositorio Institucional de la Universitat de Valéncia
instname
Popis: Background and objective: Anomalies in the regulation of cyclooxygenase (COX)-1 and-2 have been described in nasal polyps of aspirin-induced asthma (AIA). Whether these anomalies are specific to nasal polyps or affect all the nasal mucosa (NM) of upper airways is still unclear. The objective of this study was to compare the COX pathway in NM of AIA patients with the NM of control subjects. Methods: Fibroblasts were isolated from NM of 5 AIA patients (AIA-NM) and 5 control subjects (control-NM). Cells were treated with 10 ng/ml IL-1b for up to 72 hours. Prostaglandin E2 (PGE2) production was measured by ELISA, expression of COX-1 protein by Western blot, and COX-2 protein by ELISA, Western blot and immunofluorescence techniques. Results: IL-1b increased PGE2 production and COX-1 protein expression in control-NM fibroblasts, but no changes were found in AIA-NM. IL-1b provoked a significant timedependent increase in COX-2 protein expression in control-NM fibroblasts but had a very mild effect on COX-2 protein expression in AIA-NM. Conclusions: Our data suggest that abnormalities in the COX pathway are not a phenomenon exclusive to nasal polyp mucosa as they are also present in all the nasal mucosa of AIA patients. These anomalies may be involved in the pathogenesis of airway inflammation and NSAID intolerance in asthma patients with chronic rhinosinusitis and nasal polyposis.
Databáze: OpenAIRE