A recent basic science study (P Morey et al. Gastroenterol 2018; 154: 1391-1404) explains one of the mechanisms whereby Helicobacter pylori survives in the stomach.

The researchers used MKN45 gastric epithelial cells and human gastric cells obtained from patients undergoing gastric resections and exposed them to H pylori strains. They did additional studies in infected mice.

This report has a number of cool figures demonstrating that H pylori blocks the assembly of interferon and other cytokines.  Infected gastric cells were depleted of cholesterol which rendered them unable to respond properly to inflammatory signals from immune cells.  H pylori is able to decrease inflammation at sites of colonization while inducing inflammation in adjacent noninfected epithelium.  The authors note that patients with increased serum cholesterol (especially LDL) are at increased risk for severe H pylori gastritis.

Big Creek Greenway, Alpharetta