title: Apoptosis in Helicobacter pylori gastritis is related to cagA status.
abstract: BACKGROUND
  Helicobacter pylori infection increases gastric epithelial cell apoptosis; however, the influence of cagA status is still controversial. We aimed to investigate if cagA status is related to apoptosis in H. pylori gastritis at different anatomic sites of the gastric mucosa.
  
  
  METHODS
  We studied by immunohistochemistry (streptavidin-biotin method) pro-apoptotic (Bax and Bak) and antiapoptotic (Bcl-2 and Bcl-x) proteins expression, scored from 0 to 4, in gastric biopsies, at the antrum (lesser and greater curvatures), incisura, and corpus (greater curvature) from 50 patients with H. pylori gastritis (22 males, 28 females, median age 40 years) and eight non-infected patients (6 males, median age 39.6 years). H. pylori and cagA status were determined by polymerase chain reaction.
  
  
  RESULTS
  Apoptotic proteins were expressed in a granular pattern, in the cytoplasm of foveolar cells; Bax and Bak expression was higher than Bcl-2 and Bcl-x in most cases and was significantly higher in patients infected by cagA-positive strains than in those infected by cagA-negative strains (p = .001). Bak expression was higher at the lesser curvature (antrum and incisura) than in the other regions (p = .002) and was correlated with atrophy. Anti-apoptotic proteins were significantly more expressed at the antral lesser curvature than in the other regions of the stomach (Bcl-2: p = .02; Bcl-x: p < .001).
  
  
  CONCLUSIONS
  Infection with cagA-positive strains is significantly associated with overexpression of pro-apoptotic proteins in the gastric mucosa, mainly at the antral lesser curvature, which may have a role on atrophy development. Anti-apoptotic proteins were also overexpressed at the lesser curvature, which may occur to keep epithelial cell turnover or might be related to malignant transformation.
authors.affiliation: Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, Brazil.
authors.forename: Mônica M D A
authors.initials: MM
authors.lastname: Cabral
authors.forename: Cláudia M C
authors.initials: CM
authors.lastname: Mendes
authors.forename: Lúcia P F
authors.initials: LP
authors.lastname: Castro
authors.forename: Christiane T
authors.initials: CT
authors.lastname: Cartelle
authors.forename: Juliana
authors.initials: J
authors.lastname: Guerra
authors.forename: Dulciene M M
authors.initials: DM
authors.lastname: Queiroz
authors.forename: Ana M M F
authors.initials: AM
authors.lastname: Nogueira
mesh_terms: D000328:Adult; D000942:Antigens, Bacterial / Q000032:analysis* / Q000235:genetics; D017209:Apoptosis; D001426:Bacterial Proteins / Q000032:analysis* / Q000235:genetics; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000378:metabolism* / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori