The Relationship Between Gastric Diseases And Amino Acid Polymorphism In Caga-multimerization Sequence Of Helicobacter Pylori

Objective Helicobacter pylori infection on gastric mucosa can cause a variety ofdiseases, especially CagA-positive strains on gastric mucosal injury is more serious. CMsequence of CagA protein have multiple pathways mediated morphological changes andtumorigenesis of gastric epithelial cells. Thus, CM sequence of CagA protein as abreakthrough for the carcinogenic mechanisms CagA protein in-depth study of the system,indicating that the amino acid sequence of CM polymorphism and Helicobacter pyloriinfection related mucosal lesions, thus causing further clarify the CagA protein molecularmechanism of gastric cancer.Method275cases of gastric mucosa specimens were collected by endoscopic biopsyand H. pylori infection states of all samples were tested by four different methods, rapidurease test, HE staining, methylene blue staining and immunohistochemical staining.H.pylori genomic DNA was extracted from paraffin-embedded tissue by DNA isolationkit.The nucleotide sequencing of cagA variable regions was amplified by polymerase chainreaction and amplified products were performed gene sequencing. After gene sequenceswere translated into amino acid sequences, we analyzed the variability of amino acids fromCM sequence.Results1. The rates of H. pylori infection detected by four methods have significant differences. The positive rate of H. pylori infection by rapid urease test is32.4%(89/275), followed by HEstaining37.8%(104/275), immunohistochemistry staining58.2%(160/275) and methyleneblue staining65.8%(181/275). Methylene blue staining was sensitive in detecting H. pylorifrom gastric mucosa, but the high rate of false-positive (47.8%,55/115) indicated it was not areliable method.2. The rate of H.pylori infection in different types of gastric mucosal lesions has significantdifferences. The positive rate of H.pylori infection in gastric cancer and ulcer disease are64.7%(11/17), followed by simple gastritis62.8%(59/94), and atrophic gastritis52.3%(68/130).3. The cagA gene of H.pylori in gastric mucosa has difference. The positive rate of cagAgene is70%(77/110), which is associated with active inflammatory lesions in atrophicgastritis, cagA-positive rate of78.6%(33/43).CagA-positive strains more likely to causechronic active gastritis and gastric glandular atrophy, intestinal metaplasia serious. However,there are no significant differences in dysplasia of gastric mucosa and carcinoma byCagA-positive strains and negative strains caused.4. CM on CagA protein sequence have differences, CM sequence variation in4cases,2cases of CM in the first eight amino acid sequence of alanine mutation of glycine (A/G),1cases of the first10amino acid sequence of CM asparagine mutation of glycine (N/G),1cases of the7amino acid of CM alanine mutation of threonine （A/T）,CM sequencevariation where all of Helicobacter pylori strains from atrophic gastritis.Conclusion1The rate of H.pylori in Our group was58.2%, mainly in the East Asian type CagA straindistribution based.2HP infection and gastric mucosal lesions caused by CagA status are closely related,CagA-positive strains more likely to cause chronic active gastritis and intestinal metaplasia.3CM CagA protein sequence variation exists, the variation was5.2%.