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Research Articles

What happens to basophils and tryptase, LXA4 and CysLTs during aspirin desensitization?

, MDORCID Icon, , MDORCID Icon, , PhD, , PhD, , MD, , MD, , MD, , MD, , MD & , MDORCID Icon show all
Pages 1524-1534 | Received 20 Jul 2022, Accepted 04 Dec 2022, Published online: 30 Dec 2022
 

Abstract

Introduction

Aspirin desensitization (AD) is an effective treatment in patients with non-steroidal anti-inflammatory drugs (NSAID)-exacerbated respiratory disease (NERD) by providing inhibitory effect on symptoms and polyp recurrence. However, limited data is available on how AD works. We aimed to study comprehensively the mechanisms underlying AD by examining basophil activation (CD203c upregulation), mediator-releases of tryptase, CysLT, and LXA4, and LTB4 receptor expression for the first 3 months of AD.

Methods

The study was conducted in patients with NERD who underwent AD (group 1: n = 23), patients with NERD who received no desensitization (group 2: n = 22), and healthy volunteers (group 3, n = 13). All participants provided blood samples for flow cytometry studies (CD203c and LTB4 receptor), and mediator releases (CysLT, LXA4, and tryptase) for the relevant time points determined.

Results

All baseline parameters of CD203c and LTB4 receptor expressions, tryptase, CysLT, and LXA4 releases were similar in each group (p > 0.05). In group 1, CD203c started to be upregulated at the time of reactions during AD, and continued to be high for 3 months when compared to controls. All other study parameters were comparable with baseline and at the other time points in each group (p > 0.05).

Conclusion

Although basophils are active during the first 3 months of AD, no releases of CysLT, tryptase or LXA4 exist. Therefore, our results suggest that despite active basophils, inhibition of mediators can at least partly explain underlying the mechanism in the first three months of AD.

Acknowledgements

We thank David Chapman for the English revision of the manuscript.

Clinical trial registration

This study is registered to ISRCTN Registry (BMC, Springer Nature) with registry number ISRCTN27096541.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

Additional information

Funding

This study is supported by Ankara University Scientific Research Projects

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