The bacterium Helicobacter pylori infects the stomachs of half the world’s population. Infection can be asymptomatic in many people, but it can also lead to serious health problems, including peptic ulcers, stomach cancer and lymphoma.
Reported in Infection and Immunity, a study from Matthew Jung, Mark McClain, PhD, Holly Algood, PhD, and colleagues shows that a bacterial enzyme called Lnt is essential for H. pylori colonization in mice.
In H. pylori and other Gram-negative bacteria, Lnt is the final enzyme in a conserved three-step lipoprotein modification pathway. Lipoproteins have many functions including enabling H. pylori to adhere to the lining of the stomach and helping it evade the host’s immune response.
Treating human gastric epithelial cells with an H. pylori lipoprotein, the team found a fortified innate immune response when lipoproteins were left unmodified by Lnt. Introducing the bacterium in mice, the team found that deletion of Lnt prevents H. pylori colonization altogether. The study identifies lipoprotein synthesis as a promising target for intervention in H. pylori infection.
Others on the study include M. Blanca Piazuelo, PhD, and Lee Brackman, MPH. The study was supported in part by the National Institutes of Health (grant R21AI163586).
