CagA and VacA are immunoblot markers of past Helicobacter pylori infection in atrophic body gastritis
CagA and VacA are immunoblot markers of past Helicobacter pylori infection in atrophic body gastritis
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DOI：
10.1111/j.1523-5378.2007.00467.x
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发表时间：
2007-02-01
期刊：
影响因子：
4.4
通讯作者：
Delle Fave, Gianfranco
中科院分区：
文献类型：
--
作者：
Annibale, Bruno;Lahner, Edith;Delle Fave, Gianfranco
背景萎缩性体胃炎（ABG）可能由幽门螺旋杆菌感染引起。在这种情况下很难诊断幽门螺杆菌感染，因为在身体萎缩的过程中细菌消失了。30%的ABG患者没有检测到幽门螺杆菌感染的迹象。我们的目的是调查常规方法（ELISA血清学和吉姆萨染色组织学）分类为幽门螺杆菌阴性的ABG患者是否曾暴露于感染。方法138例ABG门诊患者，其中31例为幽门螺杆菌阴性（组织学和ELISA血清学），107例为幽门螺杆菌相关（组织学和ELISA血清学阳性：活动性感染，n = 29；血清学阳性：既往感染，n = 78）。对照组30例，组织学和ELISA血清学均为幽门螺杆菌阴性。对血清进行幽门螺杆菌全细胞蛋白裂解物免疫印迹。结果对照血清均不能识别CagA、VacA、热休克蛋白B和脲酶B，特异性为100%。所有幽门螺杆菌阴性的ABG患者均表现出免疫印迹血清反应性，包括每种病例中的CagA或VacA。与活动性感染（77.4% vs. 86.2%）和既往感染（61.5%）的ABG患者相比，幽门螺杆菌阴性患者对CagA和VacA的血清反应性非常普遍。结论针对CagA和VacA的免疫印迹能够证明所有常规方法定义为幽门螺杆菌阴性的ABG患者既往暴露于幽门螺杆菌感染，提示幽门螺杆菌感染在这些患者的胃萎缩中也有隐藏作用。
Background Atrophic body gastritis (ABG) may be induced by H. pylori infection. It is difficult to diagnose H. pylori infection in this condition, since during progression of body atrophy the bacterium disappears. In 30% of patients with ABG no sign of H. pylori infection is detectable. We aimed to investigate whether patients with ABG, classified as H. pylori-negative by conventional methods (ELISA serology and Giemsa stain histology), have been previously exposed to the infection.Methods Case series consisted of 138 outpatients with ABG, of whom 31 are H. pylori negative (histology and ELISA serology), and 107 are H. pylori related (histology and ELISA serology positive: active infection, n = 29; only serology positive: past infection, n = 78). Thirty control subjects who were H. pylori negative at histology and ELISA serology were investigated. Immunoblotting of sera against H. pylori whole-cell protein lysate was performed.Results None of the control sera recognized CagA, VacA, heat-shock protein B, and urease B, yielding a specificity of 100%. All H. pylori-negative patients with ABG showed immunoblotting seroreactivity, including in each case either CagA or VacA. The concomitant seroreactivity against CagA and VacA was highly prevalent in the H. pylori-negative patients with ABG, comparable to those with active infection (77.4% vs. 86.2%) and with past infection (vs. 61.5%).Conclusions Immunoblotting against CagA and VacA is able to prove past exposure to H. pylori infection in all patients with ABG defined as H. pylori-negative by conventional methods, suggesting a hidden role of H. pylori infection in gastric atrophy also in these patients.