Aceti A, Celestino D, Caferro M, Casale V, Citarda F, Conti E M, Grassi A, Grilli A, Pennica A, Sciarretta F
Institute of Clinic of Tropical and Infectious Diseases, La Sapienza University, Rome, Italy.
Gastroenterology. 1991 Jul;101(1):131-7. doi: 10.1016/0016-5085(91)90469-2.
The immunoglobulin (Ig) E immune response in patients with Helicobacter pylori-associated chronic gastritis has been evaluated. Of 26 patients with H. pylori infection, 22 (84%) tested positive for basophil-bound specific IgE (determined by the histamine release test) and 18 (69%) for serum specific IgE (determined by an enzyme-linked immunosorbent assay). In contrast, only 1 of 17 persons in whom the bacterium was not detected presented cell-bound and serum specific IgE. In the 4 histamine release test--positive but enzyme-linked immunosorbent assay--negative patients, removal of antibody from the basophil surface by acid elution showed that histamine release occurred through an IgE-dependent mechanism. When normal basophils, passively sensitized with serum from IgE-positive patients, were exposed to the H. pylori antigen, a significant release was observed, confirming the class specificity of the response. Inhibition experiments with bacteria other than H. pylori showed that the IgE antibody was specifically directed against this organism. The percentage of antigen-induced histamine release did not correlate with serum specific IgE level. However, the response of basophils to antigenic challenge was proportional to IgE-dependent cellular releasability. This finding suggests that target cell sensitivity may be the most important factor in determining the entity of biological response to the antigenic challenge. The ability of H. pylori to induce a specific IgE immune response could answer key questions regarding the mechanisms inducing gastric inflammation.
对幽门螺杆菌相关性慢性胃炎患者的免疫球蛋白（Ig）E免疫反应进行了评估。在26例幽门螺杆菌感染患者中，22例（84%）嗜碱性粒细胞结合特异性IgE检测呈阳性（通过组胺释放试验测定），18例（69%）血清特异性IgE检测呈阳性（通过酶联免疫吸附测定法测定）。相比之下，在17例未检测到该细菌的人中，只有1例出现细胞结合和血清特异性IgE。在4例组胺释放试验阳性但酶联免疫吸附测定阴性的患者中，通过酸洗脱从嗜碱性粒细胞表面去除抗体表明，组胺释放是通过IgE依赖性机制发生的。当用IgE阳性患者的血清被动致敏的正常嗜碱性粒细胞暴露于幽门螺杆菌抗原时，观察到显著的释放，证实了反应的类特异性。用幽门螺杆菌以外的细菌进行的抑制实验表明，IgE抗体是特异性针对该生物体的。抗原诱导的组胺释放百分比与血清特异性IgE水平无关。然而，嗜碱性粒细胞对抗原刺激的反应与IgE依赖性细胞释放能力成正比。这一发现表明，靶细胞敏感性可能是决定对抗原刺激的生物学反应性质的最重要因素。幽门螺杆菌诱导特异性IgE免疫反应的能力可以回答有关诱导胃炎症机制的关键问题。
