Vorobjova Tamara, Ren Zhigang, Dunkley Margaret, Clancy Robert, Maaroos Heidi-Ingrid, Labotkin Rait, Kull Karl, Uibo Raivo
Centre of Molecular and Clinical Medicine, Institute of General and Molecular Pathology, University of Tartu, Tartu, Estonia.
APMIS. 2006 May;114(5):372-80. doi: 10.1111/j.1600-0463.2006.apm_392.x.
Polarized immune response to Helicobacter pylori and induction of chronic inflammation may increase the risk of gastric atrophy and adenocarcinoma. We studied the association of the response of IgG1 and IgG2 antibodies to H. pylori with grade of gastric chronic inflammation and atrophy in a population with a high prevalence of H. pylori, and compared these data with the data obtained from the study of gastric cancer patients, as well as with the data for CagA positivity. Altogether, 114 persons from two adult population samples from Estonia and 45 consecutive gastric cancer patients were studied. All patients were positive for the H. pylori antibody determined by ELISA. Adenocarcinoma was classified histologically according to the Laurén's system. The response of the IgG subclasses to H. pylori (acid glycine-extracted whole cell proteins) was determined by ELISA and the results were compared with the ELISA results for the recombinant fragment of the CagA protein. Helicobacter pylori IgG level was lower in atrophic gastritis compared with nonatrophic gastritis (chronic inflammation) (p=0.001). In the group of cancer patients, the response of IgG and IgG1 was lower compared with both gastritis groups (p=0.01 and p=0.0002 for IgG, and p=0.001 and p=0.0005 for IgG1). IgG2 was lower for gastric cancer localized in the corpus (p=0.03). In conclusion, atrophic gastritis and gastric cancer were associated with a significant decline in IgG and IgG1 response to H. pylori compared with nonatrophic gastritis. Higher value of CagA antibodies was seen in gastric cancer and in gastric atrophy compared with nonatrophic gastritis; in gastric cancer patients, IgG1 response to H. pylori was correlated with CagA status.
对幽门螺杆菌的极化免疫反应以及慢性炎症的诱导可能会增加胃萎缩和腺癌的风险。我们在幽门螺杆菌高流行率人群中研究了IgG1和IgG2抗体对幽门螺杆菌的反应与胃慢性炎症和萎缩程度之间的关联，并将这些数据与从胃癌患者研究中获得的数据以及CagA阳性数据进行了比较。总共对来自爱沙尼亚的两个成人样本中的114人和45例连续的胃癌患者进行了研究。所有患者通过ELISA检测幽门螺杆菌抗体均为阳性。腺癌根据劳伦氏系统进行组织学分类。通过ELISA测定IgG亚类对幽门螺杆菌（酸性甘氨酸提取的全细胞蛋白）的反应，并将结果与CagA蛋白重组片段的ELISA结果进行比较。与非萎缩性胃炎（慢性炎症）相比，萎缩性胃炎中幽门螺杆菌IgG水平较低（p = 0.001）。在癌症患者组中，与两个胃炎组相比，IgG和IgG1的反应较低（IgG分别为p = 0.01和p = 0.0002，IgG1分别为p = 0.001和p = 0.0005）。胃体部的胃癌中IgG2较低（p = 0.03）。总之，与非萎缩性胃炎相比，萎缩性胃炎和胃癌与对幽门螺杆菌的IgG和IgG1反应显著下降有关。与非萎缩性胃炎相比，胃癌和胃萎缩中CagA抗体的值更高；在胃癌患者中，对幽门螺杆菌的IgG1反应与CagA状态相关。
