Prostaglandin E2 decrease in induced sputum of hypersensitive asthmatics during oral challenge with aspirin

Abstract

Background

A special regulatory role for prostaglandin E₂ (PGE₂) has been postulated in Nonsteroidal anti‐inflammatory drugs (NSAIDs)‐exacerbated respiratory disease (NERD).

Objective

To investigate the effect of systemic aspirin (acetylsalicylic acid) administration on airways PGE₂ biosynthesis in induced sputum supernatant (ISS) among subjects with NERD or aspirin‐tolerant asthma with chronic rhinosinusitis with nasal polyposis (ATA‐CRSwNP), as well as healthy controls (HC).

Methods

Induced sputum (IS) was collected from patients with NERD (n=26), ATA‐CRSwNP (n=17), and HC (n=21) at baseline and after aspirin challenge. Sputum differential cell count and IS supernatant (ISS) levels of prostanoids: PGE₂, 8‐iso‐PGE₂, tetranor‐PGE‐M, 8‐iso PGF₂α and leukotriene C₄, D₄ and E₄ were determined using mass spectrometry. Urinary excretion of LTE₄ was measured by ELISA.

Results

NERD subjects had elevated sputum eosinophilic count as compared to ATA‐CRSwNP and HC (median NERD 9.1%, ATA‐CRSwNP 2.1% and HC 0.4%; P<0.01). Baseline ISS levels of PGE₂ were higher in asthmatics as compared to HC at baseline (NERD vs. HC P=0.04, ATA‐CRSwNP vs. HC P<0.05). Post‐challenge ISS levels of PGE₂ compared to baseline significantly decreased in NERD and HC (P<0.01 and P=0.01), but not in ATA‐CRSwNP. In NERD a similar decrease of PGE₂ as in HC resulted from 2.8 times lower dose of aspirin.

Conclusions

Aspirin‐precipitated bronchoconstriction is associated with a decrease in airway PGE₂ biosynthesis. These results support the mechanism of PGE₂ biosynthesis inhibition as a trigger for bronchoconstriction in NERD.

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