Cytokine gene polymorphisms and Helicobacter pylori
(HP) genotypes have been linked to gastric cancer development in Western countries. We determined the role of host cytokine polymorphisms and bacterial virulent factors in the development of gastric intestinal metaplasia (IM) in a Chinese population with a high background gastric cancer incidence.
Three hundred two HP-infected noncancer individuals living in Shandong province of China with available DNA were studied. Polymorphisms in different loci of inflammatory cytokines Interleukin IL-1B, IL-1RN
, Interleukin IL-8, IL-10, IL-18
, tumor necrosis factor-A (TNF-A
), and Transforming growth factor (TGF-B)
, were determined by allelic discriminating TaqMan polymerase chain reaction (PCR) or a variable number of tandem repeats. Presence of HP virulence factors in cagA, vacA
, and babA2
were determined by PCR. Baseline gastric biopsies were assessed for the presence of IM.
Among HP-infected subjects, carriers of the IL-1B-511
T allele were associated with a modestly greater prevalence of IM (adjusted OR 2.0, 95% CI 1.0–3.7). There was no association between the presence of IM and polymorphisms in other inflammatory cytokines. Although most subjects from this region harbored the virulent HP strains, carriage of the vacA
m1 strain was associated with a significantly higher prevalence of IM (adjusted OR 1.8, 1.1–3.0). The presence of both host (IL-1B-511
T) and HP (vacA
m1) genotypes further increased the risk of IM (OR 5.7, 2.0–16) when compared with individuals with the low-risk genotype.
The carriage of proinflammatory IL-1B-511
and HP vacA
m1 genotypes was associated with the development of gastric IM in the Chinese.