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|Title:||The association between the polymorphism of the interleukin 8, 10 genes and the clinical manifestation of helicobacter pylori's infection in the Lebanese population||Authors:||Jalbout, Stephany A. Al||Advisors:||Haddad, Lara||Issue Date:||2019||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.
Includes bibliographical references (p. 60-67).
Supervised by Dr. Lara Haddad.
|URI:||https://scholarhub.balamand.edu.lb/handle/uob/4297||Rights:||This object is protected by copyright, and is made available here for research and educational purposes. Permission to reuse, publish, or reproduce the object beyond the personal and educational use exceptions must be obtained from the copyright holder||Ezproxy URL:||Link to full text||Type:||Thesis|
|Appears in Collections:||UOB Theses and Projects|
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