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Introduction: H. pylori BabA is an outer membrane protein that mediates bacterial adherence to the gastric epithelium, triggers several pathways during the course of infection, and thus contributes to the disease development. Considering the variability in the presence of BabA coding gene (babA2) among H. pylori clinical strains, the aim of this study was to assess the relationship between the genotype status of H. pylori babA2 and the severity of clinical and histopathological outcomes. Methods: Gastric mucosal biopsy specimens were collected from 30 CLO test-positive patients, 16 with gastritis and 14 with peptic ulcer disease. Polymerase chain reaction was carried out to detect the presence of H. pylori-specific glmM gene and BabA coding gene (babA2). Histopathological examination was performed to evaluate the severity of H. pylori-associated gastric disease according to the Updated Sydney Classification System. Results: The glmM and babA2 genes were present in 100% and 86.7% of the tested H. pylori strains, respectively. Although higher degrees of inflammatory activity and H. pylori density were noted in babA2-positive biopsy specimens, there was no statistically significant association between babA2 genotype status and the severity of gastric disease. Conclusion: The babA2 genotype status of H. pylori may not be considered as a sole marker for determining the infection outcomes.
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PURPOSE: Helicobacter pylori infection is probably acquired in childhood and persists as an asymptomatic infection for decades in most individuals. It is unclear why only a minority of those infected develop a clinical manifestation, even in childhood, such as peptic ulcer disease. H. pylori infection activates local immune responses and causes lymphocyte infiltration in the gastric mucosa. We have previously reported that both T and B cells in the lamina propria play important roles in the local immune response of H. pylori-infected children. The aim of this study was to investigate the association between H. pylori genotypes and gastric mucosal lymphocytes. METHODS: Twenty-five H. pylori-infected children (10 with peptic ulcer disease and 15 with gastritis) were enrolled in this study. We investigated the genotypes (cagA, cagE, vacA, and babA2) and evaluated the association with clinical manifestations, histopathology, and gastric mucosal lymphocytes. RESULTS: The prevalence of cagA, cagE, vacA s1m1, and babA2 was 80%, 60%, 84%, and 88%, respectively. The most prevalent (68%) combination of cagA, vacA, and babA2 genotypes was cagA+/ vacA s1m1+/babA2+. H. pylori genotypes were not associated with clinical manifestations, histopathology, or gastric mucosal lymphocytes. CONCLUSION: There was no association between the cagA, cagE, vacA, or babA2 status and gastric mucosal lymphocytes. The role of the host immune response in relation to H. pylori genotypes and disease potential in children needs further studies.
Subject(s)
Child , Humans , Asymptomatic Infections , B-Lymphocytes , Gastric Mucosa , Genotype , Helicobacter , Helicobacter pylori , Lymphocytes , Mucous Membrane , Peptic Ulcer , PrevalenceABSTRACT
Objective To investigate the possible influence of Lewis B expression in Helicobacter pylori (H.pylori) on bacterial adhesion property, and determine the relationship between babA 2 gene in H.pylori and peptic ulcer. Methods The bacterial adhesion property in a total of 78 H.pylori strains was performed using adherence assay in vitro, and the frequency of babA 2 gene was determined by polymerase chain reaction (PCR). Results Among 47 H.pylori strains isolated from peptic ulcer patients, 18 (38.3%) were positive for babA 2 gene, while babA 2 was positive in 14 (45.2%) of 31 strains isolated from non ulcer dyspepsia patients ( P =0.427). Among 31 H.pylori strains expressing Lewis B, 24 (77.4%) were positive for adherence assay, compared with 38 (80.9%) of 47 H.pylori strains without expression of Lewis B ( P =0.463). Conclusions (1) There is no association between babA 2 status in H.pylori strain and peptic ulcer in our population; (2) The expression of Lewis B in H.pylori does not interfere with bacterial adhesion property, and thus supports that the gastric epithelium is the receptor for Lewis B of H.pylori.
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Objective To determine the distribution of Helicobacter pylori (H.pylori) iceA, babA2 in patients in Shanghai and explore the association of H. pylori strain genotype with its clinical outcome after infection. Methods A total of 141 H. pylori strains was isolated from gastric biopsy samples of 43 patients with chronic gastritis, 47 patients with duodenal ulcer (DU), 30 patients with gastric ulcer(GU) and 21 patients with non cardia gastric carcinoma. The iceA, vacA, cagA, and babA2 genotypes were determined by polymerase chain reaction (PCR). Results iceA1, iceA2 and babA2 were detected in 74.5% (105/141) , 15.6% (22/141) and 63.8% (90/141) of the 141 H.pylori strains, respectively, while 2 of isolated H. pylori strain (1.4%) were positive for both iceA alleles and 16(11.3%) were negative for both iceA alleles. The prevalence of babA2 and the combined genotype of babA2 and cagA in H. pylori isolated from DU patients were significantly higher than that in GU patients (74.5% vs. 50.0% for babA2, P =0.028; 70.2% vs. 46.7% for babA2 and cagA, P =0.039). There was no significant difference in prevalence of babA2 among other disease groups. No association of different clinical diseases with iceA genotype was detected. Conclusions The most common genotype of H.pylori strains isolated from patients in Shanghai is iceA1 +/babA2 +. babA2 may play different role in the pathogenesis of duodenal ulcer and gastric ulcer. No association between iceA status and clinical outcome of H.pylori infection was confirmed in our study.