Helicobacter pylori Induce Col1a1 Up-Regulation, DNA Damage, and Fibrosis in Gastric Precancerous Lesions

Helicobacter pylori (H. pylori) induces gastric precancerous lesions (GPL), but their underlying biomarkers remain poorly characterized. To establish a GPL model, BALB/c mice were inoculated with H. pylori via gavage. Immunofluorescence confirmed successful modeling by detecting H. pylori distribution and aberrant expression of precancerous lesion markers. Serum-based label-free proteomics and bioinformatic analyses were performed to screen key proteins. Data are available via ProteomeXchange (PXD076808). Western blot and immunofluorescence were used to verify key proteins and markers of DNA damage, fibrosis, and epithelial mesenchymal transition (EMT). The results revealed high H. pylori load in gastric mucosa with abnormal precancerous markers. Proteomic analysis identified 103 differentially expressed proteins and five core proteins as potential biomarkers, all overexpressed in gastric cancer. Col1a1, a fibrosis marker, was identified as a key upregulated protein and validated by Western blot and immunofluorescence. Col1a1 colocalized with the DNA damage marker γ-H2AX in gastric mucosa. H. pylori infection triggered DNA damage, fibrosis, and EMT in GPL. In conclusion, H. pylori induced DNA damage, fibrosis, and EMT in gastric mucosa, accelerating precancerous lesion progression, with Col1a1 playing a significant role.