Abstract：
BACKGROUND: Outer membrane protein (OMP) of Helicobacter pylori (H. pylori) i.e., blood group antigen binding adhesin (babA) is responsible for the attachment of H. pylori in the gastric epithelium. Its adherence is causative for gastric pathology such as gastritis, peptic ulcer disease (PUD), or digestive tract disorders like erosive reflux disease (ERD) and (NERD) non-erosive reflux disease and together called Gastroesophageal reflux disease (GERD). BabA manifests rapid and varied selection via substitution of amino acid in its Leb-carbohydrate binding domain (CBD) which enables better binding preferences for distinct human populations and ABO blood group phenotypes. The positive evolutionary selection of the pathogenic factor of this genetically diverse bacterium has enabled it to adapt to the host gastric environment. Analyzing the association of virulent genes (cagA, vacA) and babA will help us better understand bacteria\'s pathogenicity.
METHODS: 109 H. pylori strains from patients with distinct gastrointestinal diseases were genotyped using Polymerase Chain Reaction(PCR) for cagA, vacA, and babA followed by Sanger sequencing and phylogenetic analysis.
RESULTS: In the babA + ve genotype, a statistically significant association with p = 0.04 and < 0.0001 is seen in gastritis and ERD respectively. A significant association of genotype vacAs1m2 (p = 0.0002) was seen in gastritis, vacAs1m1 (p = 0.02) in NERD, vacAs1m1 (p < 0.0001) and vacAs1m2 (p = 0.002) in ERD. This relationship helps to detect gastritis or ERD where BabA gene can be used as an independent marker for detecting their presence.
CONCLUSIONS: The appearance of variants within distinct disease categories is due to local genetic variation.
METHODS: 109 H. pylori strains from patients with distinct gastrointestinal diseases were genotyped using Polymerase Chain Reaction(PCR) for cagA, vacA, and babA followed by Sanger sequencing and phylogenetic analysis.
RESULTS: In the babA + ve genotype, a statistically significant association with p = 0.04 and < 0.0001 is seen in gastritis and ERD respectively. A significant association of genotype vacAs1m2 (p = 0.0002) was seen in gastritis, vacAs1m1 (p = 0.02) in NERD, vacAs1m1 (p < 0.0001) and vacAs1m2 (p = 0.002) in ERD. This relationship helps to detect gastritis or ERD where BabA gene can be used as an independent marker for detecting their presence.
CONCLUSIONS: The appearance of variants within distinct disease categories is due to local genetic variation.
摘要：
背景：幽门螺杆菌的外膜蛋白（OMP）（H。幽门螺杆菌)，即血型抗原结合粘附素（babA）负责幽门螺杆菌在胃上皮中的附着。它的坚持是胃病的原因，如胃炎，消化性溃疡病（PUD），或消化道疾病，如糜烂性反流病（ERD）和非糜烂性反流病（NERD），统称为胃食管反流病（GERD）。BabA通过取代其Leb-碳水化合物结合域（CBD）中的氨基酸表现出快速和变化的选择，这使得能够更好地结合不同人群和ABO血型表型。这种遗传多样性细菌的致病因子的积极进化选择使其能够适应宿主胃环境。分析毒力基因(cagA，vacA）和babA将帮助我们更好地了解细菌的致病性。
方法：109H。来自不同胃肠道疾病患者的幽门螺杆菌菌株使用聚合酶链反应（PCR）对cagA进行基因分型，vaca,然后是Sanger测序和系统发育分析。
结果：在babA+ve基因型中，在胃炎和ERD中分别观察到p=0.04和<0.0001的统计学显着相关。在胃炎中发现基因型vacAs1m2（p=0.0002）的显着关联，vacAs1m1（p=0.02）在NERD，在ERD中vacAs1m1(p<0.0001)和vacAs1m2(p=0.002)。这种关系有助于检测胃炎或ERD，其中BabA基因可以用作检测其存在的独立标记。
结论：不同疾病类别中变异的出现是由于局部遗传变异。
方法：109H。来自不同胃肠道疾病患者的幽门螺杆菌菌株使用聚合酶链反应（PCR）对cagA进行基因分型，vaca,然后是Sanger测序和系统发育分析。
结果：在babA+ve基因型中，在胃炎和ERD中分别观察到p=0.04和<0.0001的统计学显着相关。在胃炎中发现基因型vacAs1m2（p=0.0002）的显着关联，vacAs1m1（p=0.02）在NERD，在ERD中vacAs1m1(p<0.0001)和vacAs1m2(p=0.002)。这种关系有助于检测胃炎或ERD，其中BabA基因可以用作检测其存在的独立标记。
结论：不同疾病类别中变异的出现是由于局部遗传变异。
