Determination of Enzymatic Antioxidant in Iraqi Patients with Chronic Gastritis

Abstract

Infection of the gastric mucosa with Helicobacter pylori is strongly associated with chronic gastritis, peptic ulcer and gastric cancer. Helicobacter pylori virulence factors include a variety of proteins that are involved in its pathogenesis, such as VacA and CagA. Another group of virulence factors is clearly important for colonization of H.pylori in the gastric mucosa. These include urease, motility factors (flagellin), and Superoxide dismutase (SOD). Because of this organism's microaerophilic nature and the increased levels of reactive oxygen in the infected host, we expect that other factors involved in the response to oxidative stress are likely to be required for virulence. Superoxide dismutase is a nearly ubiquitous enzyme among organisms that are exposed to toxic environments. In this study, we measured the SOD in serum of 80 patients complain from chronic gastritis and infected with H.pylori. 37 patients infected with H.pylori have the CagA gene, and 13 patients are not and also measured the SOD in 30 control groups that not infected with H.pylori. Serum level of SOD was significantly (p<0.05) higher in patients with chronic gastritis compared to controls. Also significantly higher (p<0.001) in patients with chronic gastritis infected with H.pylori positive CagA than patients infected with H.pylori negative CagA.
 Key words: chronic gastritis, H.pylori, CagA, SOD
 الخلاصــة

Gingival tissue samples from periodontitis patients demonstrate epithelial–mesenchymal transition phenotype

“…IRS of E‐cadherin was interpreted as previously described; 30 0–1 (negative), 2–3 (mild), 4–8 (moderate), 9–12 (strongly +). While IRS of Snail1 was divided into low expression (0–3) and high expression (4–12) as previously described 31 …”

“…6,7 The sequelae of EMT result in discontinuity of the coherent epithelial sheets and increased populations of more motile fibroblasts. 8 The main promoters of EMT include gram-negative bacteria, inflammatory cytokines, smoking, oxidative stress, and hypoxia [9][10][11] which are shared risk factors between EMT and periodontitis. 12 Notably, EMT processes can be reversed by removing the chronic stimuli or by using EMT inhibitors.…”

Pathogenesis of periodontitis – A potential role for epithelial-mesenchymal transition

“…Persistent exposure of gastric epithelium to H. pylori has been shown to result in morphological changes indicative of mesenchymal-like cells [132] . In addition, specific toxins and virulence factors from this bacterium, e.g., CagA, are can induce morphological changes and increase cellular migratory ability [133] , [134] , [135] . These data support the role of H. pylori as a major risk factor for gastric and duodenal ulceration and gastric carcinoma which potentially act via EMT-induction [136] , [137] .…”