Scientific publications
Nonsteroidal anti-inflammatory drugs enhance IgE-mediated activation of human basophils in patients with food anaphylaxis dependent and independent of nonsteroidal anti-inflammatory drugs. Scientific Publication
Pascal M (1,2), Muñoz-Cano R (2,3), Milà J (1), Sanz ML (4), Diaz-Perales A (5), Sánchez-López J (2,3), García-Moral A (2,3), Juan M (1,2), Valero A (2,3), Yagüe J (1,2), Picado C (2,3), Bartra J (2,3).
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 (Flow2 CAST™ , 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.
CITATION Clin Exp Allergy. 2016 Mar 28. doi: 10.1111/cea.12735