Abstract
Background: Fibroblasts from nasal polyps (NP) of asthma patients have reduced expression of cyclooxygenase 2 (COX-2) and production of prostaglandin E2 (PGE2). We hypothesized that the reported alterations are due to alterations in the availability of arachidonic acid (AA). Objective: The objective was to determine the fatty acid composition of airway fibroblasts from healthy subjects and from asthma patients with and without aspirin intolerance. Methods: We analyzed the fatty acid composition of cultured fibroblasts from non-asthmatics (n = 6) and from aspirin-tolerant (n = 6) and aspirin-intolerant asthmatics (n = 6) by gas chromatography-flame ionization detector. Fibroblasts were stimulated with acetyl salicylic acid (ASA). Results: The omega-6 fatty acids dihomo-gamma-linolenic acid (C20:3) and AA (C20:4), and omega-3 fatty acids docosapentaenoic acid (DPA) (C22:5) and docosahexaenoic acid (DHA) (C22:6) were significantly higher in NP fibroblasts than in fibroblasts derived from nasal mucosa. The percentage composition of the fatty acids palmitic acid (C16:0) and palmitoleic acid (C16:1) was significantly higher in fibroblasts from patients with NP and aspirin intolerance than in fibroblasts derived from the nasal NP of aspirin-tolerant patients. ASA did not cause changes in either omega-3 or omega-6 fatty acids. Conclusions. Our data do not support the hypothesis that a reduced production of AA in NP fibroblasts can account for the reported low production of PGE2 in nasal polyps. Whether the increased proportion of omega-3 fatty acids can contribute to reduced PGE2 production in nasal polyps by competitively inhibiting COX-2 and reducing the amount of AA available to the COX-2 enzyme remains to be elucidated.
Highlights
Asthma is a syndrome characterized by the presence of chronic inflammation, resulting in airway obstruction and bronchial hyper-responsiveness that causes wheezing, coughing, and dyspnea [1].Nasal polyposis (NP) is a chronic inflammatory disease of the sinus mucosa usually seen in association with chronic rhinosinusitis (CRS) and asthma [2]
Our data do not support the hypothesis that a reduced production of arachidonic acid (AA) in NP fibroblasts can account for the reported low production of prostaglandin E2 (PGE2) in nasal polyps
The omega-6 fatty acids, dihomo-gamma-linolenic acid (C20:3) and AA (C20:4), and the omega-3 fatty acids, docosapentaenoic acid (DPA) (C22:5) and docosahexaenoic acid (DHA) (C22:6), were significantly higher in nasal polyp fibroblasts than in fibroblasts derived from nasal mucosa
Summary
Asthma is a syndrome characterized by the presence of chronic inflammation, resulting in airway obstruction and bronchial hyper-responsiveness that causes wheezing, coughing, and dyspnea [1]. Nasal polyposis (NP) is a chronic inflammatory disease of the sinus mucosa usually seen in association with chronic rhinosinusitis (CRS) and asthma [2]. The pathogenesis of CRS with NP is related to an altered inflammatory state that results in a tissue remodeling process [3]. Aspirin-intolerant asthma (AIA) is a distinct syndrome characterized by asthma, CRS, NP, and aspirin sensitivity. The pathophysiological mechanism of AIA is only partially understood and appears to be related to anomalies in the metabolism of arachidonic acid AA [4,5]. We hypothesized that the reported alterations are due to alterations in the availability of arachidonic acid (AA)
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