Interleukin-10 (−819 C/T) and Tumor Necrosis Factor-α (−308 G/A) Gene Variants Influence Gastritis and Lymphoid Follicle Development

Helicobacter pylori (H. pylori) causes gastritis, development of lymphoid follicles and later monoclonal mucosa-associated lymphoid tissue (MALT) lymphoma. We evaluated the association of tumor necrosis factor (TNF)-α (−308 G/A) and IL-10 (−819 C/T) gene polymorphisms with gastritis and lymphoid follicle formation. H. pylori infection was detected using modified Giemsa staining and IgG anti-CagA enzyme-linked immunosorbent assay (ELISA). One hundred and thirty patients with non-ulcer dyspepsia (NUD) and 200 healthy age-matched controls were genotyped for TNF-α and IL-10 polymorphisms using polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP). Subjects with IL-10 −819 T allele [patients (46.5%) versus controls (35.7%), p = 0.006, OR = 1.56, 95% CI = 1.14–2.15] were at risk of gastritis. Infection with H. pylori was more often associated with lymphoid follicles formation than its absence (46% versus 22%, p = 0.009). TNF-α polymorphism did not influence gastritis but patients with TNF-α −308 A allele carriers showed >2 fold risk of lymphoid follicle formation [presence (26%) versus absence (11.25%), p = 0.029, OR = 2.8; 95% CI = 1.09–7.08]. There was a trend towards association of lymphoid follicles and TNF-α −308 A allele carriers with H. pylori infection than without (58.5% versus 22.2%; p = 0.064). IL-10 −819 T and TNF-α −308 A alleles may increase risk of gastritis and lymphoid follicle formation.