Correlation between HP infection-induced peptic ulcers accompanied with gastric precancerous lesions and LC3B

Autophagy is one lysosome-dependent degradation process. It can degrade damaged structures inside cytoplasm, producing amino acids and free fatty acids, thus acclimating cells for anorexia and hungry environments. Autophagy is modulated by various signaling pathways, whose dysregulation is closely correlated with tumor, aging and degeneration. This study aims to investigate the correlation between Helicobacter pylori (HP) infection accompanied with gastric precancerous lesions and autophagy. A total of 263 peptic ulcers patients who were diagnosed by gastroscopy and mucosal biopsy were recruited. Semi-quantitative RT-PCR and Western blotting were employed to quantify expression of autophagy factor LC3B. HP assay was performed by 14C inhalation test. The correlation between HP positive rate and expression level of LC3B was analyzed, along with the correlation between precancerous lesion in gastric ulcers by HP infection and LC3B level. LC3B was significantly correlated with HP infection, atypical atrophy of gastric epithelial cells, chronic atrophic gastritis and intestinal metaplasia. Logistic regression revealed correlation between LC3B level with HP infection (OR=5.05, 95% CI: 1.14~23.45, P=0.02). There was a correlation between autophagy factor LC3B over-expression and HP infection along with gastric ulcers accompanied with atypical atrophy of gastric mucous.