Helicobacter pylori vacA genotype is a predominant determinant of immune response to Helicobacter pylori CagA

Figure 1 Difference in Sydney score and Helicobacter pylori seropositivity in patients with and without anti-CagA-IgG. Mean histological scores ± SD. A: Activity; B: Chronicity, C: Atrophy; D: Intestinal metaplasia are shown; E: Anti-Helicobacter pylori IgG; F: anti-CagA-IgG titer were evaluated using ELISA; Statistical analyses were performed using Mann-Whitney test.

Figure 2 Correlation between anti-CagA-IgG and anti-Helicobacter pylori IgG and vacA s/m polymorphisms. A: Quantitative values for anti-Helicobacter pylori IgG and anti-CagA-IgG were correlated in patients with positive serology (n = 30) using Pearson’s test; B: Patients with available data to vacA s1/2m1/2 polymorphisms were divided in subgroups dependent on s/m subtype. Anti-CagA-IgG values were sorted in increasing order. Dotted line shows the cut-off for seropositivity of the test (6.25 U/mL).

Figure 3 Inflammatory potential based on CagA-IgG in gastric mucosa ex vivo and in vitro using AGS cells. A: IL-8 mRNA expression was evaluated in antrum mucosa from patients with chronic gastritis [CG, AG, IM, without peptic ulcer disease (PUD) and gastric cancer (GC)] with (n = 23) and without CagA seropositivity (n = 48); B: IL-8 expression in antrum mucosa from patients with PUD and gastric cancer (n = 4 for CagA-IgG+ and n = 6 CagA-IgG-); C: IL-8 mRNA; D: IL-8 protein expression in supernatant are shown for subgroups dependent on cagA, cagA mRNA and anti-CagA-IgG status in vitro using co-culturing of Helicobacter pylori strains from patients with AGS cells.

Figure 4 Inflammatory potential of Helicobacter pylori strains in relation to vacA polymorphism. Helicobacter pylori strains from patients were co-cultivated with AGS cell and A-B: IL-8 mRNA; C-D: IL-8 expression in supernatant were measured using qPCR and ELISA.