Nonsteroidal anti-inflammatory drugs enhance IgE-mediated activation of human basophils in patients with food anaphylaxis dependent and independent of nonsteroidal anti-inflammatory drugs

Abstract

Background

Nonsteroidal anti-inflammatory drugs (NSAIDs) act as co-factors worsening the allergic reactions induced by food allergens.

Aim

To evaluate the effect of both lysine acetylsalicylate (L-ASA) (non-selective cyclooxygenase (COX) inhibitor) and valdecoxib (selective COX-2 inhibitor) in basophils activated by peach Lipid Transfer Protein (Pru p 3) in patients with food-dependent NSAID-induced anaphylaxis (FDNIA).

Methods

Twenty Pru p 3 allergic patients with FDNIA group, eleven peach anaphylaxis not exacerbated by NSAIDs (no-NSAIDs group), and 5 healthy volunteers were recruited. Basophil activation (BA) was measured as expression of CD63 (Flow²CAST^™, Bühlmann^®), after stimulation with Pru p 3, both alone and in combination with L-ASA (1.13, 3.38 and 6.78 mM) or valdecoxib (0.87, 7.8 and 31.25 μM).

Results

Basophils from no-NSAID group were significantly more reactive and sensitive to Pru p 3 than those from the FDNIA group. In both groups, an increase in BA was observed when basophils were exposed to Pru p 3 and L-ASA. In the FDNIA group, valdecoxib partially abrogates the BA induced by Pru p 3, whereas in the no-NSAID group, a dual effect was observed depending on the concentration tested.

Conclusions

This study indicates that subjects with food-induced anaphylaxis differ from FDNIA subjects in the higher reactivity and sensitivity of their basophils to allergen challenge. We have shown a direct effect of NSAIDs on basophils using a human model of FDNIA. Our results also suggest that selective COX2 inhibitors might be a safe alternative. BA test may be a useful tool in the study of the pathogenic mechanism of the cofactor phenomenon.

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