title: [The heterogeneity of genetic variants of Helicobacter pylori in patients with various acid-related diseases].
abstract: OBJECTIVE
  To study the genetic diversity of H. pylori in patients with chronic gastritis, peptic ulcer disease, chronic pancreatitis.
  
  
  METHODS
  The study involved 490 patients with gastric ulcer, duodenal ulcer, chronic superficial gastritis, chronic atrophic gastritis, chronic pancreatitis. Diagnosis of H. pylori infection was carried out by the following methods: morphological, urea breath test serological (determining the concentration of IgG antibodies to H. pylori and immunoblotting) and by polymerase chain reaction. For genotyping of H. pylori using sets of primers with a mixture of CagA, VacA s1/ s2, VacA m1, VacA m2, IceA1, IceA2, BabA. To perform immunoblotting using Anti-Helicobacter pylori EUROLINE-Western blot (IgG), based on the Western blot method using test strips with antigens separated by electrophoresis cell extract H. pylori. Statistical computer processing was performed using software packages Statistic for Windows 6.0.
  
  
  RESULTS
  The virulent genotype of H. pylori was determined in 92% cases of duodenal ulcer. In chronic non-atrophic and atrophic gastritis virulent genotypes of H. pylori were not detected. In case of uncomplicated duodenal ulcer we revealed isolated (vacA m2) and combined (vacA s1/ s2) genotypes of H.pylori in 23% of cases, of them monogenotip VacAm2 (vacuolating-associated cytotoxin) was determined in 83%. In complicated duodenal ulcer the combined genotype of H. pylori (vacAs1/ s2; vacAs1/ s2 + vacAm1 + vacAm2; vacAs1/ s2 + vacAm2) and mixed genotype of H. pylori (vacAs1/ s2 + cagA, vacAs1/ s2 + iceA2, vacAm1 + cagA + iceA2) were determined in 77% of the samples. In cases of chronic pancreatitis the vacuolating cytotoxin VacA was detected in 35.7%, such as in the control group it was 81.8%. Genes encoding the production of urease (subunit A) were found in 85.7% of chronic pancreatitis patients, in the control group--54.5%. Genes encoding the synthesis of outer membrane proteins of H. pylori such as p26, p19, p17 were detected in 82.1% of patients with chronic pancreatitis, in patients of the control group--54.5%. H. pylori outer membrane proteins with molecular weights of 30 and 33kDa (p30 and p33) were detected in 85.7% of patients with chronic pancreatitis.
  
  
  CONCLUSIONS
  The bacterium H. pylori, which is the main cause of acid diseases, realizes effect through its pathogenicity factors. Waste products of H. pylori have a direct damaging effect on the mucous membrane of the stomach and duodenum, contributing to the release of lysosomal enzymes, a number of cytokines. They are cause the development of inflammatory processes in the mucosa. Lipopolysaccharide of outer membrane of H. pylori cause immune response of the human body and the development of chronic inflammation at the system level. Set of pathogenicity factors of H. pylori determine the nature and severity of the pathological processes triggered by the bacterium at different levels of the microorganism.
authors.forename: E V
authors.initials: EV
authors.lastname: Domracheva
authors.forename: A S
authors.initials: AS
authors.lastname: Sarsenbaeva
authors.forename: K A
authors.initials: KA
authors.lastname: Ufimtsev
mesh_terms: D016022:Case-Control Studies; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology; D005756:Gastritis / Q000378:metabolism / Q000382:microbiology*; D014644:Genetic Variation; D060005:Genotyping Techniques; D016481:Helicobacter Infections / Q000378:metabolism / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000302:isolation & purification / Q000472:pathogenicity; D006801:Humans; D050500:Pancreatitis, Chronic / Q000378:metabolism / Q000382:microbiology*; D010437:Peptic Ulcer / Q000378:metabolism / Q000382:microbiology*; D014774:Virulence / Q000235:genetics