The association between cagL and cagA, vacAs/m, babA genes in patients with gastric cancer, duodenal ulcer, and non-ulcer dyspepsia related to Helicobacter pylori

Introduction : As a component of the cag T4SS, the cagL gene is invoked in the translocation of CagA into host cells and is essential for the formation of cag PAI-associated pili between H. pylori and gastric epithelial cells. Aim : We aimed to investigate the clinical association of the cagL gene with other virulence Factors (VacA, CagA, EPIYA-C, and BabA protein) of GC, pylori strains isolated from GC, duodenal ulcer (DU), and non-ulcer dyspepsia (NUD) cases. Methods : The patient group (PC), including 47 patients (22 GC and 25 DU) and a 25 control group (CG= NUD) were included. Amplification of the H. pylori cagL, cagA, vacA, and babA2 genes and typing of EPIYA motifs were performed by PCR methods. Results : Sixty-one (84.7%) H. pylori strains were detected with cagL (93.6% in SG, 68% in CG). We detected a significant difference between SG and (1; for the presence of cagL (p=0.012) but no statistical comparison was done for (>= 2) EPIYA-C repeats In the comparison of H. pylori strains with cagA/vacAs1m1 and cagA/vacAs1m2 and babA2 for the presence of cagL we could not detect a significant difference (p=1). Conclusion : We detected a significant difference between groups for the presence of cagL genotype (p=0.012). The vacAs1m1 (OR: 2.829), genotypes increased the GC and DU risk by 2.8 times, while multiple (>= 2) EPIYA-C repeats incresed the GC and DU risk by 3.524 times. Gender (to be female) (OR: 0.454) decreased the GC and DU risk by inversly decreased in the multivariate analysis.