H Pylori Screening, Eradication May Prevent Development of Colorectal Cancer

Helicobacter pylori (H pylori) infection is a strong causal promoter of colorectal carcinogenesis that should factor into colorectal cancer (CRC) risk calculation, suggests a study published in the journal Gut.

“Eradication of H pylori infection might be an effective measure to reduce this risk,” wrote corresponding author Markus Gerhard, MD, a professor in the school of medicine at Technical University of Munich in Germany, and study coauthors.

To better understand the causal and functional connection between H pylori infection and colon cancer, researchers infected two Apc-mutant mouse models and C57BL/6 mice with H pylori and analyzed changes in intestinal immune responses and epithelial signatures.

Infection with H pylori hastened the development of tumors in Apc-mutant mice, according to the study.

“We identified a unique H pylori-driven immune alteration signature characterized by a reduction in regulatory T cells and pro-inflammatory T cells,” researchers wrote. “Furthermore, in the intestinal and colonic epithelium, H pylori induced pro-carcinogenic STAT3 signaling and a loss of goblet cells, changes that have been shown to contribute — in combination with pro-inflammatory and mucus degrading microbial signatures — to tumor development.”

Biopsies of colons from people with H pylori infection showed similar immune and epithelial alterations, researchers noted.

However, early eradication of H pylori infection with antibiotic triple therapy consisting of clarithromycin, metronidazole, and omeprazole normalized tumor incidence in mice to the same levels as in uninfected controls, the study found.

“We suggest H pylori screening and eradication as a potential measure for CRC prevention strategies,” researchers wrote.

Reference:
Ralser A, Dietl A, Jarosch S, et al. Helicobacter pylori promotes colorectal carcinogenesis by deregulating intestinal immunity and inducing a mucus-degrading microbiota signature. Gut. 2023;72(7):1258-1270. doi:10.1136/gutjnl-2022-32807