Prostaglandin E2in Induced Sputum Following Oralaspirin Challenge in Asthma Patients with and without Aspirin Hypersensitivity
Sunday, March 6, 2016
South Exhibit Hall H (Convention Center)
Lucyna Mastalerz, MD, PhD, Maria Ignacak, MD, Michal Buczek, MD, Aleksandra Cholewa, MD, Natalia Celejewska-Wojcik, MD, Krzysztof Wojcik, MD, PhD, Anna Gielicz, MSc, Krzysztof Oles, MD, PhD, Marek Sanak, MD,PhD
Rationale: Induced sputum (IS) supernatant allows to measure lipid mediators of asthmatic inflammation in bronchial secretions. The specific role of endogenous bioactive prostaglandin E2(PGE2) in aspirin-induced asthma (AIA) is not well understood.  

Methods: To investigate theinfluence of aspirin on sputum supernatant concentration of PGE2 during aspirin challenge, using chromatography-mass spectrometry measurements in subjects with AIA (n=26) and aspirin-tolerant asthma (ATA, n=17), and healthy controls (HC, n=21).ISwas collected before and following oral aspirin challenge. Sputum differential cell count and sputum supernatant concentrations of PGE2were assessed.

Results: Aspirin precipitated bronchoconstriction in all AIA subjects, but in none of the ATAand HC. Phenotypes of asthma based on the sputum cytology  differed between the groups. The IS specimens were mainly eosinophilic in AIA and paucigranulocitic in HC. In ATA group non phenotype based on the sputum cytology was dominant. At baseline, mean sputum supernatant concentrations of PGE2was higher in asthma patients independent of aspirin hypersensitivity as compared to HC. Following the challenge, PGE2decreased in all study groups (ANOVA, p<0,001).However, this decrease was statisticallysignificant only in AIA patients(p=0.01) and HC.A cumulativedose of aspirin had no effect on the magnitude of the PGE2 alterations. 

Conclusions: PGE2decreases significantly in AIA during the oral challenge.The results support theory on the inhibition of PGE2 biosynthesis as a trigger for bronchoconstriction mediated by cysteinyl leukotrienes in AIA.