The relationship between virulence factors of Helicobacter pylori and severity of gastritis in infected patients.
The outcome of Helicobacter pylori infection has been related to specific virulence-associated bacterial genotypes. The best known genotypic virulence factors of H. pylori are cytotoxin-associated gene A (cagA) and vacuolating cytotoxin gene A (vacA). The objective of this study was to assess the relationship between H. pylori cagA and vacA status and histopathological findings. Esophagogastrodoedonoscopy was performed in 80 dyspeptic patients. Antrum and corpus biopsies were obtained for isolation of H. pylori and for histopathological assessment. The polymerase chain reaction was used to detect cagA and vacA genes of H. pylori using specific primers. Biopsy samples were stained with hematoxylin and eosin, and histopathological findings were graded using the "updated Sydney system". H. pylori from 57 of the 80 patients was incubated. Of the 57 patients, 44 were cagA positive. In the corpus biopsy specimens there was a significant relationship between the density of H. pylori colonization (P = 0.02) and chronic inflammation (P = 0.02) and cagA-positive genotypes. In the antrum specimens there was a significant relationship between cagA positivity and neutrophil activity (P = 0.003) and glandular atrophy (P = 0.002), but not with H. pylori density, chronic inflammation, and intestinal metaplasia. The odds ratio of cagA-positive vs. cagA-negative strains for the presence of glandular atrophy, irrespective of grading and of gastric localization, was 4.62 (95% CI, 1.18-18.08, P = 0.041). No significant relationships were observed between vacA s1 and s2 genotypes and histopathological parameters. Corpus neutrophil infiltration was found to be more severe in the m1 group than in the m2 group (P = 0.004). Other histopathological features showed no difference between m1 and m2 genotypes. In conclusion H. pylori strains showing cagA positivity are associated with more severe gastritis in some histological features but virulence factors of H. pylori do not appear to determine the overall pattern of gastritis.
Umit
Hasan
H
Department of Gastroenterology, Trakya University Medical Faculty, Edirne, Turkey, 22030. drhumit@gmail.com
Tezel
Ahmet
A
Bukavaz
Sebnem
S
Unsal
Gulbin
G
Otkun
Muserref
M
Soylu
Ali Riza
AR
Tucer
Dilek
D
Otkun
Metin
M
Bilgi
Selcuk
S
D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics* / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011706:Pyloric Antrum / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D012720:Severity of Illness Index; D014421:Turkey; D037521:Virulence Factors / Q000235:genetics* / Q000378:metabolism; D055815:Young Adult
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori; D037521:Virulence Factors; C080866:cagA protein, Helicobacter pylori