Prostaglandins, leukotrienes, and other arachidonic acid metabolites in nasal polyps and nasal mucosa

Abstract

Prostaglandins (PGs) and leukotrienes (LTs) are known to play an important role in allergic inflammatory reactions. The triad of aspirin sensitivity, nasal polyposis, and asthma led us to suspect that PGs, LTs and other arachidonic acid metabolites may be involved in the pathogenesis of nasal polyps. The purpose of this study was to determine arachidonic acid metabolites and to measure concentrations of PGs and LTs in nasal polyps and nasal mucosa. Samples of nasal polyps and nasal mucosa were obtained at the time of polypectomies and nasal procedures. Metabolites of arachidonic acid in tissue were determined by incubation of tissue-homogenates with 14C-arachidonic acid and analyses with thin-layer chromatography and high performance liquid chromatography (HPLC). Levels of PGE2, 6-keto-PGF1 alpha, thromboxane (Tx)B2, 15-hydroxyeicosatetraenoic acid (HETE), LTC4, LTB4 were measured by radioimmunoassay. The predominant arachidonic acid metabolite in both nasal polyps and mucosa with 15-HETE. The HPLC analysis showed that the predominant metabolite in nasal polyp was 15-HETE, especially in polyps from aspirin sensitive patients. Levels of 15-HETE and PGE2 were higher in polyps from patients with a history of allergy than from nonallergic patients. Levels of LTC4 and LTB4 in nasal polyps were determined. The findings of this study will help to explain biochemical basis of the pathogenesis of aspirin-sensitive nasal polyps and to develop better medical treatment for them.

Tissue remodelling in upper airways: where is the link with lower airway remodelling?

“…Increased concentrations of cysteinyl leukotrienes are released from the polypoid upper airway mucosa and enzymes involved in leukotriene production (5-lipoxygenase and LTC4 synthase) are overexpressed in the mucosa of patients with rhinosinusitis (63,64). Urinary excretion of LTE4 in patients with CRS and nasal polyposis is increased in relation to the extend of the disease and decreases after the sinus surgery (65).…”

The So-Called ‘Allergic’ Nasal Polyp

“…Others advocate the view that allergic dis eases are no more common in patients with polyps than in the normal population and that allergy is an unlikely cause of nasal polyps [14][15][16][17][18], Several different mecha nisms and possible relationships for the development of nasal polyps have been proposed, e.g. a release of media tors from mast cells [19,20], multiple immunological mechanisms [21], or the influence of leukotrienes and inhibition of prostaglandin synthesis [22,23]. and a cellmediated immune response via activated T cells [24], In the present study, and attempt is made to enlighten whether nasal polyps are associated with nasal allergy and allergy-like conditions, and whether these diseases are causative in the development of the nasal polyp.…”

Evidence of Platelet-Activating Factor in Nasal Polyps

“…PGs and LTs were detected in nasal polyps from patients with chronic sinus itis and nasal allergy. Interestingly, the amount of LTs was increased in nasal polyps from patients with aspirininduced asthma [12], In nasal polyps, arachidonic acid is converted to PGs and LTs [21 ]. PAF is a potent mediator of allergy and inflammation, and a close link between the production of arachidonic metabolites and PAF has been demonstrated [22], We examined nasal polyps from patients with chronic sinusitis and detected PAF activity in all the polyps.…”