Pantic Ivana, Lugonja Sofija, Jerotic Djurdja, Pljesa-Ercegovac Marija, Matic Marija, Bakovic Nikola, Vojnovic Marko, Simic Tatjana, Milovanovic Tamara, Savic-Radojevic Ana
Clinic for Gastroenterology and Hepatology, University Clinical Center of Serbia, 11000 Belgrade, Serbia.
Division of Gastroenterology, Department of Internal Medicine, General Hospital "Djordje Joanovic", 23000 Zrenjanin, Serbia.
Int J Mol Sci. 2025 Jan 9;26(2):488. doi: 10.3390/ijms26020488.
Considering the mutual relationship between redox disbalance and inflammation in (HP) infection, we aimed to evaluate whether the polymorphisms in antioxidant glutathione transferases genes ( rs1695, rs1138272, rs4925 and rs156697) modify susceptibility to HP infection, as well as the severity of HP-associated gastric manifestation development. Therefore, GST gene polymorphisms were determined via the appropriate PCR in 101 HP-positive and 107 HP-negative patients. Our results show that carriers of the variant genotype (rs1695) or at least one variant allele (rs1138272) were more prone to the development of HP-positive gastritis compared with reference allele carriers (OR = 3.21, 95%CI = 1.15-8.91, = 0.025 and OR = 2.31, 95%CI = 1.14-4.89, = 0.021, respectively), which was confirmed by haplotype analysis. HP-positive carriers of the *A variant allele showed increased risk of developing gastric atrophy and precancerous gastric lesions compared with the reference one (OR = 2.49, 95%CI:1.04-5.96, = 0.04 and OR = 2.98, 95%CI = 1.21-7.34, = 0.018, respectively). HP-positive carriers of the *G variant allele were less prone to developing moderate/severe inflammatory infiltration (OR = 0.35, 95%CI = 1.04-5.96, = 0.04), whereas the *T variant allele was significantly associated with active inflammation (OR = 4.09, 95%CI = 1.04-5.96, = 0.042). In conclusion, antioxidant GST genetic propensity seems to have an important impact on both acute and chronic forms of HP infection.
考虑到氧化还原失衡与幽门螺杆菌（HP）感染炎症之间的相互关系，我们旨在评估抗氧化谷胱甘肽转移酶基因（rs1695、rs1138272、rs4925和rs156697）的多态性是否会改变对HP感染的易感性，以及HP相关胃部表现发展的严重程度。因此，通过适当的聚合酶链反应（PCR）对101例HP阳性和107例HP阴性患者进行了谷胱甘肽转移酶（GST）基因多态性检测。我们的结果显示，与参考等位基因携带者相比，变异基因型（rs1695）携带者或至少一个变异等位基因（rs1138272）携带者更易发生HP阳性胃炎（优势比[OR]=3.21，95%置信区间[CI]=1.15 - 8.91，P=0.025；OR=2.31，95%CI=1.14 - 4.89，P=0.021），单倍型分析证实了这一点。与参考等位基因携带者相比，*A变异等位基因的HP阳性携带者发生胃萎缩和癌前胃部病变的风险增加（OR=2.49，95%CI：1.04 - 5.96，P=0.04；OR=2.98，95%CI=1.21 - 7.34，P=0.018）。G变异等位基因的HP阳性携带者发生中度/重度炎症浸润的可能性较小（OR=0.35，95%CI=1.04 - 5.96，P=0.04），而T变异等位基因与活动性炎症显著相关（OR=4.09，95%CI=1.04 - 5.96，P=0.042）。总之，抗氧化GST基因倾向似乎对HP感染的急性和慢性形式都有重要影响。
