Targeted mobilization of Lrig1 ⁺ gastric epithelial stem cell populations by a carcinogenic Helicobacter pylori type IV secretion system

Significance Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma and has been deemed a class I carcinogen by the World Health Organization. One of the most important H. pylori virulence factors is the cag pathogenicity island (PAI); however, the precise mechanisms through which H. pylori induces gastric adenocarcinoma are incompletely defined. In human samples, Lrig1 expression is enhanced in lesions with premalignant potential. In mouse models, chronic H. pylori infection stimulates Lrig1 + progenitor cells in a cag -dependent manner, and these stem cells give rise to differentiated gastric cells. Thus, the cag PAI is a key mediator of the epithelial progenitor cell responsiveness that develops following chronic H. pylori infection.