Peanut-specific IgE antibodies in asymptomatic Ghanaian children possibly caused by carbohydrate determinant cross-reactivity.

Peanut-specific IgE antibodies in asymptomatic Ghanaian children possibly caused by carbohydrate determinant cross-reactivity.
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DOI:
10.1016/j.jaci.2013.04.023
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发表时间:
2013-09
影响因子:
14.2
通讯作者:
Yazdanbakhsh, Maria
Yazdanbakhsh, Maria
中科院分区:
医学1区
文献类型:
--
作者:
Amoah, Abena S.;Obeng, Benedicta B.;Larbi, Irene A.;Versteeg, Serge A.;Aryeetey, Yvonne;Akkerdaas, Jaap H.;Zuidmeer, Laurian;Lidholm, Jonas;Fernandez-Rivas, Montserrat;Hartgers, Franca C.;Boakye, Daniel A.;van Ree, Ronald;Yazdanbakhsh, Maria

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在发达国家,花生过敏的流行率有所增加,但对花生消费量高和寄生虫感染广泛的发展中国家知之甚少。我们试图调查加纳的花生过敏。在加纳学龄儿童(n = 1604)的横断面调查中,收集了报告的花生不良反应,花生致敏(血清特异性IgE和皮肤反应),消费模式和寄生虫感染的数据。在一个子集(n = 43)IgE对阿糖胞苷h 1,2,3和9以及交叉反应性碳水化合物决定簇(CCD)的测定使用ImmunoCAP。分别通过免疫CAP抑制和嗜碱性粒细胞组胺释放研究交叉反应性和生物活性。1.5%的参与者报告了花生的不良反应,2.0%的参与者报告了皮肤点刺试验反应,17.5%的参与者报告了IgE致敏(≥0.35 kU/L)。花生致敏者(≥ 0.35kU/L)92.4%花生皮肤点刺试验阴性。埃及血吸虫感染与IgE致敏呈正相关(校正比值比,2.29; 95%CI,1.37-3.86)。在亚组中,除了6个对Ara h 9的中等强度反应外,对Ara h 1、2、3和9的IgE滴度较低(<1.3 kU/L)。抗花生的IgE与抗CCDs的IgE密切相关(r = 0.89,P <0.0001),并且几乎完全被CCDs以及S-血红蛋白可溶性卵抗原所抑制。此外,花生IgE的生物活性较差。寄生虫诱导的IgE对CCD可能占很大比例高IgE水平花生在我们的研究人群中的加纳学童。没有发现IgE介导的花生过敏的证据。
The prevalence of peanut allergy has increased in developed countries, but little is known about developing countries with high peanut consumption and widespread parasitic infections. We sought to investigate peanut allergy in Ghana. In a cross-sectional survey among Ghanaian schoolchildren (n = 1604), data were collected on reported adverse reactions to peanut, peanut sensitization (serum specific IgE and skin reactivity), consumption patterns, and parasitic infections. In a subset (n = 43) IgE against Ara h 1, 2, 3, and 9 as well as cross-reactive carbohydrate determinants (CCDs) was measured by using ImmunoCAP. Cross-reactivity and biological activity were investigated by means of ImmunoCAP inhibition and basophil histamine release, respectively. Adverse reactions to peanut were reported in 1.5%, skin prick test reactivity in 2.0%, and IgE sensitization (≥0.35 kU/L) in 17.5% of participants. Moreover, 92.4% of those IgE sensitized to peanut (≥0.35 kU/L) had negative peanut skin prick test responses. Schistosoma haematobium infection was positively associated with IgE sensitization (adjusted odds ratio, 2.29; 95% CI, 1.37-3.86). In the subset IgE titers to Ara h 1, 2, 3, and 9 were low (<1.3 kU/L), except for 6 moderately strong reactions to Ara h 9. IgE against peanut was strongly correlated with IgE against CCDs (r = 0.89, P < .0001) and could be almost completely inhibited by CCDs, as well as S haematobium soluble egg antigen. Moreover, IgE to peanut showed poor biological activity. Parasite-induced IgE against CCDs might account largely for high IgE levels to peanut in our study population of Ghanaian schoolchildren. No evidence of IgE-mediated peanut allergy was found.
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