Molecular mimicry by Helicobacter pylori CagA protein may be involved in the pathogenesis of H-pylori-associated chronic idiopathic thrombocytopenic purpura
Molecular mimicry by Helicobacter pylori CagA protein may be involved in the pathogenesis of H-pylori-associated chronic idiopathic thrombocytopenic purpura
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DOI：
10.1046/j.1365-2141.2003.04735.x
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发表时间：
2004-01-01
影响因子：
6.5
通讯作者：
Tanizawa, Y
中科院分区：
文献类型：
--
作者：
Takahashi, T;Yujiri, T;Tanizawa, Y
幽门螺杆菌的根除通常会导致慢性特发性血小板减少性紫癜（cITP）患者的血小板恢复。尽管临床观察提示H. pylori感染，对cITP的发病机制知之甚少。我们初步研究了H.幽门螺杆菌根除对20例日本成人cITP患者血小板计数的影响。然后，使用血小板洗脱液作为免疫印迹分析中的探针，我们研究了分子模拟在cITP发病机制中的作用。在75%（15/20）的cITP患者中检测到幽门螺杆菌感染。根除13例（87%）。幽门螺杆菌阳性患者，其中7例（54%）在治疗后4个月内显示血小板计数增加。完全应答的患者血小板相关免疫球蛋白G（PAIgG）水平也显著下降。12例（9例H. pylori阳性和3例H. pylori阴性）患者识别H.在三名完全缓解的患者中，根除治疗后血小板洗脱液中的抗CagA抗体水平下降。PAIgG与H. pylori CagA蛋白的表达表明CagA的分子模拟在cITP患者的发病机制中起关键作用。
The eradication of Helicobacter pylori often leads to platelet recovery in patients with chronic idiopathic thrombocytopenic purpura (cITP). Although this clinical observation suggests the involvement of H. pylori, little is known about the pathogenesis of cITP. We initially examined the effect of H. pylori eradication on platelet counts in 20 adult Japanese cITP patients. Then, using platelet eluates as the probe in immunoblot analyses, we examined the role of molecular mimicry in the pathogenesis of cITP. Helicobacter pylori infection was detected in 75% (15 of 20) of cITP patients. Eradication was achieved in 13 (87%) of the H. pylori-positive patients, seven (54%) of which showed increased platelet counts within the 4 months following treatment. Completely responsive patients also showed significant declines in platelet-associated immunoglobulin G (PAIgG) levels. Platelet eluates from 12 (nine H. pylori-positive and three H. pylori-negative) patients recognized H. pylori cytotoxin-associated gene A (CagA) protein, and in three completely responsive patients, levels of anti-CagA antibody in platelet eluates declined after eradication therapy. Cross-reactivity between PAIgG and H. pylori CagA protein suggests that molecular mimicry by CagA plays a key role in the pathogenesis of a subset of cITP patients.