This result indicates that this serum factors involved in aspirin-induced histamine expression are not mediated by IgE

This result indicates that this serum factors involved in aspirin-induced histamine expression are not mediated by IgE. release were significantly up-regulated by aspirin, they were not affected by anti-IgE antibodies. These results suggest that a single SNP of (C344C T) is usually less likely to develop AICU and the basophil activation activity in the sera by measuring CD203c expression can be applicable to confirm the diagnosis of AICU. to diagnose NSAID-induced CU except for provocation with NSAIDs = 19)= 12)Value= 0.019) (Table 2). This result excludes the role of FcRI polymorphism (C344C T) in AICU patients, and may be more specific for IgE-related airway allergies. Table 2 The genotype and allele frequency of the promoter gene of (FcR1 C66T C, rs2251746 and C334C T, rs242782). = 20)= 50)= 52)ValueNCAAvalue for the HardyCWeinberg equilibrium patients in question. 2.2. Differences in Basophil Activation Activity in the Sera between the Patients with AICU and Control Group Differences in basophil activation activity in the sera between the patients with AICU (= 17) and control group (= 11) were compared by CD203c expression and histamine release. KU812 cells were incubated with aspirin and the patients sera in the presence or absence of anti-IgE antibody followed Tectorigenin by the measurement of CD203c expression and histamine release. Even though MFI of CD203 expression was similar between the two groups, the expression was only significantly up-regulated by aspirin in the subjects with AICU (108.6 2.8 122.5 5.2) and not in control group (107.0 5.1 103.3 3.1). The up-regulated CD203c expression by aspirin was not affected by anti-IgE antibody (Table 3). These results indicated that this up-regulation of CD203c and histamine release by aspirin was not IgE mediated. The percentage of histamine release was also higher in the subjects with AICU compared with control group (31.3% 7.4% ?24.0% 17.5%; 0.05) (Table 3). For evaluating KU812 cells using in expression of Tectorigenin CD203c and basophil histamine releasing assay, we performed ROC curve analysis (AUC: 0.813, 0.001) and the sensitivity and specificity were 75% and 80%, respectively. Even though histamine release was down-regulated by anti-IgE, it did not reach a statistically significant level. Table 3 Differences in basophil activation activity in sera between the subjects with AICU and those not allergic to aspirin. = 17)= 11) 0.05 analyzed by the MannCWhitney U test; c,d, 0.05 analyzed by the MannCWhitney U test; d,f, 0.05 in Mobp comparison with control by the = 7) with and without airway allergy were compared. Basophils were incubated with aspirin and the patients sera in the presence or absence of anti-IgE antibody, followed by measurement of CD203c expression and histamine release. The MFI of CD203c expression was up-regulated by aspirin in both groups, however, there was no significant up-regulation in those without airway allergy. The up-regulation of MFI in both groups was not affected by anti-IgE antibody (Table 4). The significant up-regulation of CD203c was also not inhibited by anti-IgE antibody, suggesting that basophil activation activity in the sera was not mediated by IgE. There was Tectorigenin also no statistical significance in histamine release between the subjects with and without airway allergy, despite the up-regulation of CD203c expression in those with airway allergy (Table 4). Even though histamine release was decreased by anti-IgE antibody, there was no statistically significant inhibition by anti-IgE in either group. Table 4 Differences in basophil activation activity in.