Αρχειοθήκη ιστολογίου

Αλέξανδρος Γ. Σφακιανάκης
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5
Άγιος Νικόλαος Κρήτη 72100
2841026182
6032607174

Τρίτη 1 Αυγούστου 2017

The effect of allergen-induced bronchoconstriction on concentration of 5-oxo-ETE in exhaled breath condensate of house dust mite-allergic patients

Abstract

Background

Arachidonic acid metabolites regulate several aspects of airway function including inflammation, muscle contraction and mucous secretion.

Objective

The aim of this study was to evaluate concentration of selected 5-lipoxygenase (LOX) and cyclooxygenase (COX)-derived eicosanoids in exhaled breath condensate (EBC) during allergen induced bronchoconstriction.

Methods

The study was performed on 24 allergic rhinitis/asthma patients sensitized to a house dust mite (HDM) Dermatophagoides pteronyssinus (Dp) and 13 healthy controls (HCs). Bronchial challenge with Dp extract was performed only in the allergic patients. Exhaled breath condensate (EBC) samples were collected before (T0) and during Dp-induced bronchoconstriction (TEAR). Eicosanoid concentration was measured using HPLC-tandem mass spectrometry.

Results

Significant bronchoconstriction after Dp challenge was demonstrated in 15 patients (Rs) while in 9 patients (NRs) no asthmatic response could be detected. At T0 the most abundant eicosanoids in EBC of HDM-allergic patients were LTB4 and 5-oxo-ETE while in HCs EBC concentration of LTB4 was significantly greater than that of 5-oxo-ETE. Allergen challenge resulted in significant increase in EBC concentration of 5-oxo-ETE, LTD4 and 8-iso-PGE2 only in Rs. At TEAR, the relative change of 5-oxo-ETE concentration in EBC correlated with decrease of peripheral blood eosinophilia (R= -0.774; p=0.0012). Moreover, the relative increase of 5-oxo-ETE in EBC at TEAR significantly correlated with the severity of the subsequent late asthmatic response (R=0.683 p=0.007).

Conclusion

Our study demonstrates significant up-regulation of 5-oxo-ETE synthesis in HDM-allergic patients and indicates possible involvement of that mediator in the pathogenesis of allergic asthma.

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