The association between the polymorphism of the interleukin 8, 10 genes and the clinical manifestation of helicobacter pylori's infection in the Lebanese population

Abstract

Background: Helicobacter pylori (H. pylori) is a Gram negative bacteria that colonizes almost half of the worlds population; it is associated with many gastric diseases such as peptic ulcer, gastric adenocarcinoma and gastric lymphoma. During its presence in the stomach, the bacterium releases its protein virulent factors Cag A and Vac A leading to inflammation, phagocytosis and apoptosis. The release of these toxins triggers an inflammatory response by stimulating the secretion of interleukin 8 and later on the secretion of interleukin 10 as an anti-inflammatory cytokine. Host genetic polymorphism has been implicated in having different consequences when infected by this microorganism, leading to different manifestation of Helicobacter pylori. Objective: The aim of the study was to determine the probable association between the polymorphism of IL-8 and IL-10 and the clinical manifestation in Lebanese infected people with H. pylori. Methods: 59 fresh gastric biopsies (antrum and corpus) were obtained from patients during esophagogastroduodenoscopy. The infection by H. pylori was confirmed by the polymerase chain reaction (PCR) using Cag A, Vac A s1/s2 and Vac A m1/m2 primers. The level of expression of IL-8 was detected by RT-PCR in parallel with GAPDH used as loading control, ratios of IL-8/ GAPDH were done using "Image J" software and polymorphism was checked by PCR-RFLP- and sequencing was analyzed using "Finch TV" software. Results: H. pylori genotypes were detected in 15 patients out of 59 (25.5%) where the mean age is 55.13: 60% females vs 40% males. No patients showed Cag A virulent factor, while 100% positive for Vac A s1/s2 and 86.5% for Vac A m1/m2. 40% of the patients showed epigastric pain as indication for endoscopy while 33% for epigastralgia and the remaining for epigastric pain and RGO (13.5%) vs anemia (13.5%). All patients showed an expression of IL-8 chemokine with difference in the expression level depending on the Vac A genotype. No polymorphism was seen through RFLP when using MfeI while only 3 patients showed a substitution of the "T" for the "A" nucleotide at position -251 of IL-8 promoter region. Conclusion: From our study we can conclude that there is no correlation between polymorphism in IL-8 cytokine and the clinical manifestation of Helicobacter pyloris infection, meaning no interaction between IL-8 and the prognosis of this bacterium; instead, Vac A genotype is affecting the expression level of IL-8, thus inflammation, hence progression of H. pylori.