Abstract
ABSTRACTObjectives: To determine the role of Bcl2 and p53 gene expression in the pathogenesis of antral-predominant non-atrophic gastritis (APNG) accordingto Helicobacter pylori (HP) cytotoxin-associated gene A (CagA) status.Methods: Multiple antral biopsies were taken from 78 patients for rapid urease test, histopathology, Bcl2 and P53 immunohistochemistry and HPCagA in situ hybridization.Results: CagA was detected in 74.35% cases. There was no significant difference in Bcl2 expression among CagA+ and CagA− APNG cases. Significantdifferences in polymorphonuclear neutrophils (PMNs) and lymphocytes grades were detected among CagA+ and CagA− APNG cases. There was nosignificant correlation among patients’ age, inflammatory infiltrates, Bcl2, p53 expression. CagA has positive correlation with p53 (p=0.001), PMNsgrade (p=0.027), lymphocytes grade (p=0.003), inflammation intensity (p=0.006), and inflammation activity (p=0.007). Bcl2 has no significantcorrelation with p53, CagA, PMNs, and lymphocytes indexes. P53 expression has significant correlation with PMNs and lymphocyte grades (p=0.000),inflammation intensity (p=0.003), and inflammation activity (p=0.002). PMNs grade has positive correlation with lymphocyte grade, inflammationintensity, and activity (p=0.000). Lymphocyte grade has a significant correlation with inflammation intensity and activity (p=0.000). Inflammationintensity has a significant correlation with inflammation activity (p=0.000).Conclusions: CagA cytotoxin has direct effect on P53 gene and indirect effect on Bcl2 gene expression in APNG cases. Bcl2 and P53 expression donot get affected by patient’s age and gender. PMNs grade, lymphocytes grade, inflammation intensity, and inflammation activity affected directly byP53 and CagA cytotoxin expression and indirectly by Bcl2 expression. The balance of P53-Bcl2 pathways play a vital role in pathogenesis of HP andCagA-induced APNG.Keywords: Antral-predominant non-atrophic gastritis, Bcl2, p53, Helicobacter pylori, Cytotoxin-associated gene A.
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