ATG16L1 Single Nucleotide Polymorphism Confers High Cardiac Artery Disease Risk in H. Pylori Chronic Gastritis Patients

Abstract

AbstractBackground: Chronic Helicobacter pylori (HP) gastritis affects two-thirds of the world's population and is one of the most common chronic inflammatory disorders of humans, the infection clearly results in chronic mucosal inflammation in the stomach and duodenum which in turn might lead to abnormalities in gastroduodenal motility and sensitivity and is the most frequent cause of dyspepsia and peptic disease. The increased inflammatory response related to HP gastroin-testinal disease may also lead to damage in non-gastrointestinal tissues. The damage caused by HP is believed to be associated with increased inflammatory markers resulting from immune response and blood cells activation. Autophagy related gene 16 like 1 single nucleotide polymorphism (ATG16L1 SNP) may be associated with impaired autophagy which predisposes to HP persistence and chronicity. Chronic infection is a suspected risk factor for cardiac artery disease.Aim of Study: The aim of this study is to assess the association between (ATG16L1) SNP and coronary artery disease, pro-inflammatory and atherogenic risk factors in HP patients.Patients and Methods: This study was carried out on 80 patients suffering from dyspepsia and reflux symptoms. According to the urea breath test results, patients were divided into two groups: group I (45 positive H. pylori) patients and group II (35 negative H. pylori) patients as control group. All patients were subjected to full medical history taking, clinical examination and laboratory investigations included urea breath testing for H. pylori infection, complete blood count (CBC), (ATG16L1) SNP, pro-inflammatory HDL assay and high sensitivity CRP (hs-CRP) assay.Results: H. pylori gastritis patients with AG+GG genotypes had statistically higher levels of hs-CRP, N/L, P/L, pro-oxidant HDL-c index when compared to H. pylori gastritis patients with AA genotype and both patient groups had higher levels of these parameters when compared to healthy control subjectsConclusion: The ATG16L1 SNP impairs autophagy and has a role in persistence of H. pylori intracellular infection leading to chronic gastritis and increases the CAD pro-inflammatory pro-atherogenic risk factors; the mutant G allele is accused allele.