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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 LXA 4 , and LTB 4  receptor expression for the first 3 months of AD. 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 LTB 4  receptor), and mediator releases (CysLT, LXA 4,  and tryptase) for the relevant time points determined. All baseline parameters of CD203c and LTB 4  receptor expressions, tryptase, CysLT, and LXA 4  releases were similar in each group ( p  &gt; 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  &gt; 0.05). Although basophils are active during the first 3 months of AD, no releases of CysLT, tryptase or LXA 4  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.

What happens to basophils and tryptase, LXA 4 and CysLTs during aspirin desensitization?