Expression of nuclear factor-κB1/P105 in Helicobacter pylori-induced gastric lesions

Background and aim The current study aimed to assess the proliferative activity of gastric epithelium in Helicobacter pylori ( H. pylori ) associated lesions through immunohistochemical tissue localization of NF-κB1/p105. Patients and methods Forty seven gastric specimens were included in this study as follows: 33 chronic gastritis specimens (24 H. pylori associated and nine H. pylori negative); seven gastric cancer (GC) specimens; and seven specimens from areas adjacent to GC. H. pylori intensity, gastric activity, chronicity, intestinal metaplasia, and glandular atrophy were assessed and graded by the Sydney system and correlated with NF-κB1/p105 expression. Results Gastric epithelial cells in H. pylori negative specimens expressed NFκB1/p105 as weak heterogeneous cytoplasmic staining without nuclear positivity and served as a control for immunostaining. Nuclear positivity was found in 83.3% of H. pylori gastritis, 71.4% of areas adjacent to cancer lesions and in 100% of GC lesions. The mean values of the NFκB1/p105 nuclear labeling index were significantly increased in H. pylori gastritis (46.83 ± 30.43) ( P P P H. pylori -negative controls (0 ± 0). Conclusion It is concluded that aberrant activation of NF-κB1 plays an important role in H. pylori associated gastritis, precancerous, and cancerous lesions. Hence, methods of inhibiting NF-κB signaling may have potential therapeutic application in cancer and inflammatory diseases. A better understanding of the molecular mechanisms would contribute toward both prevention and treatment of gastric carcinoma.