Sampson H A, Broadbent K R, Bernhisel-Broadbent J
Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
N Engl J Med. 1989 Jul 27;321(4):228-32. doi: 10.1056/NEJM198907273210405.
Patients with hypersensitivity to food documented by a double-blind, placebo-controlled oral food challenge have been reported to have a high rate of release of histamine from basophils in vitro. To determine whether patients with atopic dermatitis and food hypersensitivity had similar high rates of spontaneous histamine release in vitro, whether dietary elimination of relevant food antigens affected this release, and whether a cytokine, histamine-releasing factor, could account for it, we evaluated 63 patients with atopic dermatitis and food hypersensitivity (38 of whom had eliminated the offending foods from their diets), 20 patients with atopic dermatitis without food hypersensitivity, and 18 normal volunteers. Patients with atopic dermatitis and food hypersensitivity were found to have higher rates of spontaneous release of histamine from basophils than controls (mean +/- SE, 35.1 +/- 3.9 percent vs. 2.3 +/- 0.2 percent; P less than 0.001). Those who had eliminated the offending food allergen from the diet for an extended period had a significantly lower rate of histamine release (3.7 +/- 0.5 percent; P less than 0.001). In patients with atopic dermatitis without food hypersensitivity, the rate (1.8 +/- 0.2 percent) did not differ from that in normal controls. Mononuclear cells from persons with food allergies spontaneously produced a histamine-releasing factor in vitro that provoked the release of histamine from the basophils of other food-sensitive persons, but not from those of normal controls. Patients who adhered to a restricted diet had a decline in the rate of spontaneous generation of the factor by their mononuclear cells. The histamine-releasing factor was found to activate basophils through surface-bound IgE. We conclude that in patients with food hypersensitivity, exposure to the relevant antigens produces a cytokine (histamine-releasing factor) that interacts with IgE bound to the surface of basophils, causing them to release histamine.
据报道，通过双盲、安慰剂对照口服食物激发试验确诊为食物过敏的患者，其嗜碱性粒细胞在体外释放组胺的比例很高。为了确定特应性皮炎伴食物过敏的患者在体外是否也有类似的高比例自发性组胺释放，饮食中去除相关食物抗原是否会影响这种释放，以及一种细胞因子——组胺释放因子——是否可以解释这种现象，我们评估了63例特应性皮炎伴食物过敏的患者（其中38例已从饮食中去除了致敏食物）、20例无食物过敏的特应性皮炎患者和18名正常志愿者。结果发现，特应性皮炎伴食物过敏的患者嗜碱性粒细胞自发性释放组胺的比例高于对照组（均值±标准误，分别为35.1±3.9%和2.3±0.2%；P<0.001）。那些长期从饮食中去除致敏食物过敏原的患者组胺释放比例显著降低（3.7±0.5%；P<0.001）。在无食物过敏的特应性皮炎患者中，该比例（1.8±0.2%）与正常对照组无差异。食物过敏患者的单核细胞在体外可自发产生一种组胺释放因子，该因子可促使其他食物敏感者的嗜碱性粒细胞释放组胺，但不能促使正常对照组的嗜碱性粒细胞释放组胺。坚持严格饮食的患者其单核细胞自发产生该因子的比例下降。研究发现，组胺释放因子通过与表面结合的IgE激活嗜碱性粒细胞。我们得出结论，在食物过敏患者中，接触相关抗原会产生一种细胞因子（组胺释放因子），该因子与结合在嗜碱性粒细胞表面的IgE相互作用，导致嗜碱性粒细胞释放组胺。
