title: Helicobacter pylori genotypes may determine gastric histopathology.
abstract: The outcome of Helicobacter pylori infection has been associated with specific virulence-associated bacterial genotypes. The present study aimed to investigate the gastric histopathology in Portuguese and Colombian patients infected with H. pylori and to assess its relationship with bacterial virulence-associated vacA, cagA, and iceA genotypes. A total of 370 patients from Portugal (n = 192) and Colombia (n = 178) were studied. Corpus and antrum biopsy specimens were collected from each individual. Histopathological features were recorded and graded according to the updated Sydney system. H. pylori vacA, cagA, and iceA genes were directly genotyped in the gastric biopsy specimens by polymerase chain reaction and reverse hybridization. Despite the significant differences between the Portuguese and Colombian patient groups, highly similar results were observed with respect to the relation between H. pylori genotypes and histopathology. H. pylori vacA s1, vacA m1, cagA+ genotypes were significantly associated with a higher H. pylori density, higher degrees of lymphocytic and neutrophilic infiltrates, atrophy, the type of intestinal metaplasia, and presence of epithelial damage. The iceA1 genotype was only associated with epithelial damage in Portuguese patients. These findings show that distinct H. pylori genotypes are strongly associated with histopathological findings in the stomach, confirming their relevance for the development of H. pylori-associated gastric pathology.
authors.affiliation: Institute of Molecular Pathology and Immunology and the Faculty of Medicine, University of Porto, Porto, Portugal.
authors.forename: C
authors.initials: C
authors.lastname: Nogueira
authors.forename: C
authors.initials: C
authors.lastname: Figueiredo
authors.forename: F
authors.initials: F
authors.lastname: Carneiro
authors.forename: A T
authors.initials: AT
authors.lastname: Gomes
authors.forename: R
authors.initials: R
authors.lastname: Barreira
authors.forename: P
authors.initials: P
authors.lastname: Figueira
authors.forename: C
authors.initials: C
authors.lastname: Salgado
authors.forename: L
authors.initials: L
authors.lastname: Belo
authors.forename: A
authors.initials: A
authors.lastname: Peixoto
authors.forename: J C
authors.initials: JC
authors.lastname: Bravo
authors.forename: L E
authors.initials: LE
authors.lastname: Bravo
authors.forename: J L
authors.initials: JL
authors.lastname: Realpe
authors.forename: A P
authors.initials: AP
authors.lastname: Plaisier
authors.forename: W G
authors.initials: WG
authors.lastname: Quint
authors.forename: B
authors.initials: B
authors.lastname: Ruiz
authors.forename: P
authors.initials: P
authors.lastname: Correa
authors.forename: L J
authors.initials: LJ
authors.lastname: van Doorn
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics; D001706:Biopsy; D003105:Colombia / Q000453:epidemiology; D015169:Colony Count, Microbial; D004247:DNA / Q000235:genetics / Q000302:isolation & purification; D005260:Female; D005757:Gastritis, Atrophic / Q000382:microbiology / Q000473:pathology; D005773:Gastroscopy; D005838:Genotype; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics* / Q000254:growth & development / Q000472:pathogenicity; D006801:Humans; D007422:Intestines / Q000473:pathology; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D011174:Portugal / Q000453:epidemiology; D015995:Prevalence; D013270:Stomach / Q000382:microbiology / Q000473:pathology; D013274:Stomach Neoplasms / Q000453:epidemiology / Q000382:microbiology* / Q000473:pathology; D014774:Virulence / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori; C405087:iceA1 protein, Helicobacter pylori; D004247:DNA