Association of ATG16L1 genetic variant with Helicobacter pylori infection in Egyptian patients with chronic gastritis disease

Background

Helicobacter pylori infection remains a major risk for gastroduodenal inflammation and ulceration with capability to disrupt the defensive autophagy pathway in the gastric mucosal cell thus producing resilient infection. A single-nucleotide mutation in the autophagy gene ATG16L1 which controls the host immune responses to viruses and bacteria was identified as a risk factor for increasing survival and persistence of many microbial infections.

Aim

To assess the association of ATG16L1 T300A gene mutation with the susceptibility to H. pylori infection in patients with chronic gastritis disease.

Methods

ATG16L1 T300A mutation was determined by TaqMan genotyping allele specific discrimination real-time PCR assay applying specific primers, (rs2241880 A/G) and probes for A and G allele.

Result

Patients with mutant homozygous GG genotype was associated with a 4.5 times increase in the risk of H. pylori infection relative to the wild homozygous AA and the heterozygous AG genotypes (p value = 0.009, OR = 4.472; 95% CI, 0.07–0.74). The carriage rate of the mutant G allele was significantly higher in H. pylori positive cases (64%) relative to (42%) in H. pylori negative cases (p value = 0.002, OR = 2.455, 95% CI, 0.3 (0.09–1.01), and this was associated with about a 2.5 times increase in the risk for H. pylori infection.

Conclusion

Genetic variant ATG16L1 T300A mutation increased the risk of H. pylori infection in Egyptian patients with chronic gastritis disease.