Interleukin 1 Polymorphisms, Lifestyle Factors, and Helicobacter pylori Infection

Associations between Helicobacter pylori (HP) infection and lifestyle factors have been reported by several authors, but little is known about the host factors associated with the infection. This study aims to examine the infection rate of HP according to gene polymorphisms of interleukin (TL)‐IA, IL‐1B, and IL‐1RN, and to investigate the interactions with lifestyle factors. Subjects were 241 non‐cancer outpatients who had participated in a HP eradication program. Polymorphisms at ‐889 (T to C) of IL‐1A, at ‐31 (C to T; T allele makes a TATA box) and ‐511 (C to T) of IL‐1B, and at intron 2 (86‐bp VNTR (variable number of tandem repeats)) of IL‐1RN were genotyped by PCR (polymerase chain reaction), PCR‐RFLP (restriction fragment length polymorphism) and PCR‐CTPP (PCR with confronting two‐pair primers). It was found that IL‐1B polymorphisms at ‐31 and ‐511 were near‐completely linked, but in the opposite way to that in Caucasians; ‐31C/ ‐511T and ‐31T/‐511C alleles were dominant in the present subjects. The HP infection rate was substantially different among the genotypes of IL‐1B C‐31T; 45.2% (19/42) for the C/C, 67.7% (90/133) for the C/T, and 63.6% (42/66) for the T/T. The age‐sex adjusted odds ratio (OR) relative to the C/C genotype was 2.32 (95%CI (confidence interval), 1.10‐4.92) for the T/C genotype and 2.46 (1.06‐5.74) for the T/T genotype. The OR for the T/T genotype was significantly modified by smoking status; interaction term=14.6 (1.12‐190). The polymorphisms of IL‐1A and IL‐1RN were not associated with the infection rate. The results suggested that the T allele of IL‐1B C‐31T is associated with vulnerability to persistent HP infection, and that the vulnerability is modified by smoking.