Host gastric Lewis expression determines the bacterial density of Helicobacter pylori in babA2 genopositive infection

Abstract

Background and aims: We tested if host gastric Lewis antigens and the babA2 genotype of Helicobacter pylori correlated with clinicohistological outcome.

Methods: We enrolled 188 dyspeptic patients (45 with duodenal ulcer, 45 with gastric ulcer, and 98 with chronic gastritis) with H pylori infection, proved by culture and gastric histology, reviewed by the updated Sydney system. Gastric expression of Lewis (Le) antigens Le(a), Le(b), Le(x), and Le(y) was determined immunochemically to determine intensity (range 0-3). The corresponding 188 H pylori isolates were screened for babA2 genotype by polymerase chain reaction.

Results: All H pylori isolates had a positive babA2 genotype. We identified Le(a) in 33.5%, Le(b) in 72.9%, Le(x) in 86.2%, and Le(y) in 97.4% of biopsies from these 188 patients. Patients who expressed Le(b) had a higher H pylori density than those who did not express Le(b) (p<0.001). Among 139 patients who expressed Le(b), H pylori density increased with a higher Le(b) intensity (p<0.05). Gastric atrophy decreased with Le(b) intensity and thus resulted in lower H pylori density in the antrum (p<0.05). For the 49 patients without gastric Le(b) expression, H pylori density was positively related with Le(x) and Le(a) expression (p<0.05).

Conclusions: Taiwanese H pylori isolates are 100% babA2 genopositive. Gastric Le(b) as well as Le(x) intensity may be major determinants of H pylori density. While lacking gastric Le(b) expression, Le(x) and Le(a) were closely related to H pylori colonisation.

Figure 1

(A, B) Gastric immunohistochemical stains of Lewis antigen Le^b expression. (A) Positive staining over the surface epithelium only. (B) Diffuse staining over the intercryptal epithelium. (C, D) Gastric immunohistochemical stains of Le^x expression. (C) Positive staining over the surface epithelium only. (D) Diffuse staining over the deep glands.

Figure 2

The nucleotide sequence of the 271 bp polymerase chain reaction product gained from the self designed babA2 primers. The nucleotide sequence of the 10 randomly selected domestic strains (hp250, hp258, hp222, hp116, hp657, hp130, hp238, hp82, hp 639, and hp76) was confirmed to be babA2 in origin with >90% homology to the published sequence of the babA2 gene (afbabA2) of CCUG 17875. The 10 nucleotides (ATG AAA AAA C), representative of the babA2 gene of Helicobacter pylori, are indicated by “=”.

Figure 3

(A) Total Helicobacter pylori density (HPD) was positively correlated with an increase in Le^b intensity (*p<0.05, significant difference analysed using one way ANOVA). (B) Total Lewis number (Lewis-N) of each patient was also positively correlated with higher HPD in the stomach (one way ANOVA, p<0.05).