| Objectives:(1)To survey the prevalence of H.p.infection in lvliang area in patients with gastric disease.(2)to survey the prevalence of cagPai of these clinical isolates and their gene structure.(3)to explore the relationship between the polymorphism of cagpAI and severity of gastric disease.(4)To determine the expression level of Hsp60 in gastric mucosa from these patients.Methods:(1)under endoscope 306 patients' gastric biopsy specimens were obtained.(2)The presence of HP was determined by culture and these clinical isolates was identified by rapid urease test,oxidase test and Gram's staining.(3)The gene structure of cagPAI was determined by PCR and sequence analysis.(4)To detect the expression level of HSP60 by immunohistochemistry and image analysis system.Results:(1)The prevalence of HP in patients with gastric disease from lvliang area is 48.4%(148/306),of which 38 is superficial gastritis;36 is peptic ulcer,48 is atrophy gastritis,26 is gastric cancer.(2)of the 148 clinical isolates,140 is positive for cagA.of which 35 is superficial gastritis;34 is peptic ulcer;46 is atrophy gastritis,25 is gastric cancer;144 is positive for cagM,of which 35 is superficial gastritis,36 is peptic ulcer,47 atrophy gastritis,26 is gastritis cancer;144 is positive for cagT,of which 37is superficial gastritis,35 is peptic ulcer, 44 is atrophy gastritis,23 is gastritis cancer;141 is positive for ORF13,of which 35 is superficial gastritis,34 is peptic ulcer,46 is atrophy gastritis,26 is gastritis cancer;136 is positive for ORF10,of which 34 is superficial gastritis,33 is peptic ulcer,45 is atrophy gastritis,25 is gastritis cancer.Of which the positive rate of cagA,ORF13,ORF10 tended to ascend with the severity of gastric disease others not,but none of which has a significant different between them(P＞0.05)(3)The homogeneity between the gene structure of cagA from these clinical isolates and standard strain is 72.2%,but it all the isolates is 98.3%,among all the clinical isolates.(4)of the 148 clinical isolates,108(72.9%)is positive for complete cagPAI and 40(27.0%)is positive for part of the gene.The distribution of the cagPAI gene in the four groups is not significant difference among them(P＞0.05),include the isolates with complete or part of the cagPAI gene.(5)HSP60 was localized in the cytoplasm of inflammatory cells filtrating into the lamina propria.The expression level of HSP60 is higher in HP+ group than in the HP-one(P＜0.05).The positive expression in gastritis,peptic ulcer,atrophy gastritis,gastric cancer groups are 31.57%,41.66%,70.83%,76.92%,respectively.The expression level of the groups ascended with the severity of these disease and also it has a significant difference among them(P＜0.05).The overexpression occurrence of the HP60 is 15.78%,22.22%,47.91%and 65.38%,respectively among the four type disease.The overexpression level in the former two groups is significantly higher than it in the latter two. Conclusion:①HP clinical infection rate is 48.36%in this area.②The positive rate of cagA is 94.59%.The sequence of cagA have some differences with the standard strain.The character of CagA gene sequence from LvLing need to be researched further.③Because the cagA,cagM, cagT,ORF13,ORF10 have high the detection rates,so cagPAI is associated with the HP infection and as a sign of the HP virulence.There is no relation between the type of disease and the cagPAI.cagA can be used as the target of the cagPAI detection.we can not forecast the HP infection and the type of the HP associated gastric disease.The results support that HP infection enhanced the expression level of HSP60.The expression level of HSP60 in gastric mucosa may be as an indicator for the prognoses of there disease. |
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