Peters T M, Owen R J, Slater E, Varea R, Teare E L, Saverymuttu S
Public Health Laboratory, Chelmsford, UK.
J Clin Pathol. 2001 Mar;54(3):219-23. doi: 10.1136/jcp.54.3.219.
To investigate variation within the cag pathogenicity island (PAI) of Helicobacter pylori isolated from patients with dyspepsia in mid-Essex, and to evaluate the effect on expression of anti-CagA antibody.
Sixty two isolates of H pylori cultured from gastric biopsies were screened by specific PCR assays for the presence of cagA and other gene markers (cagD and cagE, and virD4) in the cag PAI. An enzyme linked immunosorbent assay (ELISA) kit (Viva Diagnostica helicobacter p120) was used to test for anti-CagA IgG antibody in matching sera. Isolates were also genotyped by vacuolating cytotoxin polymerase chain reaction (PCR) analysis, and tested for absence of the complete cag PAI (empty site PCR assay).
Forty one of the H pylori isolates had a cag PAI containing cagA. One strain had no cagA but other cag PAI loci were present, whereas the remaining 20 strains had no detectable cag PAI markers. Anti-CagA IgG antibody was detected in 34 sera by the ELISA assay, and when compared with the cag PAI genotype of the infecting strain, accuracy, sensitivity, and specificity were 92%, 87%, and 100%, respectively. The seven discrepant or borderline strains in the ELISA were all vacA s1 but differed in other genotypic markers.
The cag PAI was widely distributed in H pylori from patients with dyspepsia in mid-Essex who had different gastric pathologies. Infection with a strain having an uninterrupted cag PAI was associated with the presence of anti-CagA antibody in most patients. Discrepant ELISA results, mostly for elderly patients with duodenal ulcers, were attributed to cagA associated variation, particularly to the presence of mixed cagA+/cagA- cell variants in the infecting strain population. Tests for anti-CagA serum antibody were unreliable for predicting severity of clinical disease associated with H pylori infection in this series of patients.
研究从埃塞克斯郡中部消化不良患者中分离出的幽门螺杆菌的cag致病岛（PAI）内的变异情况，并评估其对抗CagA抗体表达的影响。
通过特异性PCR检测，对从胃活检组织中培养出的62株幽门螺杆菌进行筛选，以确定cag PAI中cagA和其他基因标记（cagD、cagE和virD4）的存在情况。使用酶联免疫吸附测定（ELISA）试剂盒（Viva Diagnostica幽门螺杆菌p120）检测配对血清中的抗CagA IgG抗体。通过空泡毒素聚合酶链反应（PCR）分析对分离株进行基因分型，并通过cag PAI空位PCR检测法检测是否存在完整的cag PAI。
41株幽门螺杆菌分离株含有包含cagA的cag PAI。1株菌株无cagA但存在其他cag PAI位点，而其余20株菌株未检测到cag PAI标记。ELISA检测在34份血清中检测到抗CagA IgG抗体，与感染菌株的cag PAI基因型相比，准确性、敏感性和特异性分别为92%、87%和100%。ELISA检测中7株结果不一致或处于临界值的菌株均为vacA s1，但在其他基因标记上存在差异。
cag PAI在埃塞克斯郡中部患有不同胃部疾病的消化不良患者的幽门螺杆菌中广泛分布。大多数患者感染具有完整cag PAI的菌株与抗CagA抗体的存在相关。ELISA结果不一致的情况，主要见于患有十二指肠溃疡的老年患者，归因于cagA相关变异，特别是感染菌株群体中存在混合的cagA+/cagA-细胞变体。在这组患者中，抗CagA血清抗体检测对于预测与幽门螺杆菌感染相关的临床疾病严重程度不可靠。
