title: A pilot study of Helicobacter pylori genotypes and cytokine gene polymorphisms in reflux oesophagitis and peptic ulcer disease.
abstract: Helicobacter pylori causes various diseases such as chronic gastritis, peptic ulcer and gastric cancer. While majority of the people infected with H. pylori is asymptomatic, 15-20 % of them develop such diseases. The main factors, which determine the development of H. pylori related diseases might be bacterial virulence, host genetic and environmental factors.The aim of this study was to reveal the factors that play a role in the disease development in patients with reflux esophagitis and peptic ulcer, infected with Helicobacter pylori. Environmental factors such as medical agents, smoking and body mass index were evaluated. The factors specific to bacteria such as vacA, CagA, babA and iceA virulence genotypes and the host factors such as IL-1, IL-2, IL-4, IL-6, IL-10, IL-12, interferon-γ, TNF-α, ve TGF-β1 gene polymorphisms were compared between the two groups.H. pylori infected twenty five patients with reflux esophagitis and peptic ulcer were enrolled in the study. There was no statistical difference between the two groups regarding environmental factors. IL-2 -330T +166T (p=0.037) and IL10 -1082A; -819C (p=0.049) gene polymorphisms were significantly more common in the group of patients with peptic ulcer compared to the group with reflux esophagitis. In both groups of patients, either with reflux esophagitis or peptic ulcer, multiple H. pylori virulence genotypes (cagA, vacA, babA) (mean values 74 %, 78 %, 54 % respectively) were observed.In this study, we revealed that cytokine gene polymorphisms may play a role in the development peptic ulcer while H. pylori virulence genotypes seem to be crucial for the development of associated diseases (Tab. 4, Ref. 51).
authors.forename: R A
authors.initials: RA
authors.lastname: Akdogan
authors.forename: O
authors.initials: O
authors.lastname: Ozgur
authors.forename: S
authors.initials: S
authors.lastname: Gucuyeter
authors.forename: N
authors.initials: N
authors.lastname: Kaklikkaya
authors.forename: U
authors.initials: U
authors.lastname: Cobanoglu
authors.forename: F
authors.initials: F
authors.lastname: Aydin
mesh_terms: D018829:Adhesins, Bacterial / Q000235:genetics; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics; D001425:Bacterial Outer Membrane Proteins / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics*; D016207:Cytokines / Q000235:genetics*; D004942:Esophagitis, Peptic / Q000382:microbiology*; D005260:Female; D005838:Genotype; D016480:Helicobacter pylori / Q000235:genetics*; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics; D007376:Interleukin-2 / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000382:microbiology*; D010865:Pilot Projects; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D014774:Virulence / Q000235:genetics; D055815:Young Adult
chemical_list: D018829:Adhesins, Bacterial; D000942:Antigens, Bacterial; C400429:BabA protein, Helicobacter pylori; D001425:Bacterial Outer Membrane Proteins; D001426:Bacterial Proteins; D016207:Cytokines; D007376:Interleukin-2; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori; C063113:ice nucleation protein; D016753:Interleukin-10