염증성 사이토카인 유전자 다형성이 감염후 과민성 장 증후군의 발생에 미치는 역할

Abstract

Background/Aims: Bacterial gastroenteritis is known as a risk factor of irritable bowel syndrome (IBS). Mild inflammatory stimuli can perturb the sensory-motor system of the gut and contribute to symptoms associated with IBS. Thus, it is suspected that pro- and anti-inflammatory cytokine gene polymorphisms have an important role in the development of IBS. The aim of this study was to investigate the association of genetic polymorphisms of: tumor necrosis factor α (TNF-α), interleukin-10 (IL-10), and transforming growth factor-α1 (TGF-α1) with the development of postinfectious IBS (PI-IBS). Methods: The subjects were recruited from our previous case-control study, where we investigated the incidence and risk factors of PI-IBS in patients with shigellosis during an outbreak. The presence of IBS and its subtypes were determined at 12 months after shigellosis infection using the Rome II criteria. In 13 patients with PI-IBS (group 1) with age- and sex-matched patients, 17, not having PI-IBS (group 2) and 20 normal controls (group 3), genotypes for TNF-α(-308*G/A), IL-10 (-1082*G/A) and TGF-α1 (+869*T/C, codon 10) were examined using the amplification refractory mutation system (ARMS) polymerase chain reaction (PCR). Results: Allele frequencies and genotypes for TNF-α, IL-10, and TGF-α1 were found to have no significant differences among the three groups. Comparing two groups at a time, there were also no differences between groups. Conclusions: Our findings suggest that genetic polymorphisms of TNF-α, IL-10, and TGF-α1 have no significant role in the development of PI-IBS.