چکیده (انگلیسی):

Background: Non-steroidal anti-inflammatory drugs (NSAIDs), especially aspirin, and food additives (FAs)
may exacerbate allergic symptoms in patients with chronic idiopathic urticaria and food-dependent exerciseinduced
anaphylaxis (FDEIA). Augmentation of histamine release from human mast cells and basophils by
those substances is speculated to be the cause of exacerbated allergic symptoms. We sought to investigate
the mechanism of action of aspirin on IgE-mediated histamine release.
Methods: The effects of NSAIDs, FAs or cyclooxygenase (COX) inhibitors on histamine release from human
basophils concentrated by gravity separation were evaluated.
Results: Benzoate and tartrazine, which have no COX inhibitory activity, augmented histamine release from
basophils similar to aspirin. In contrast, ibuprofen, meloxicam, FR122047 and NS-398, which have COX inhibitory
activity, did not affect histamine release. These results indicate that the augmentation of histamine release
by aspirin is not due to COX inhibition. It was observed that aspirin augmented histamine release from human
basophils only when specifically activated by anti-IgE antibodies, but not by A23187 or formyl-methionyl-leucylphenylalanine.
When the IgE receptor signaling pathway was activated, aspirin increased the phosphorylation
of Syk. Moreover, patients with chronic urticaria and FDEIA tended to be more sensitive to aspirin as regards
the augmentation of histamine release, compared with healthy controls.
Conclusions: Aspirin enhanced histamine release from basophils via increased Syk kinase activation, and
that the augmentation of histamine release by NSAIDs or FAs may be one possible cause of worsening symptoms
in patients with chronic urticaria and FDEIA.