It has been almost 20 years since the first report that infection with Helicobacter pylori increases the risk of stomach ulcers.
|Mice deficient in the VacA receptor, tyrosine phosphatase receptor type Z, did not develop ulcers.|
Now scientists have found that a receptor on stomach cells, for a toxin produced by H. pylori, mediates the signals that lead to ulceration in mice.
The H. pylori protein VacA has been singled out as a culprit for causing disease.
VacA binds to several receptors on stomach cells to gain entry to the cells, and cause damage.
Dr Masaharu Noda's team, from Okazaki, Japan, engineered mice deficient in one of the VacA receptors, the protein tyrosine phosphatase receptor type Z (Ptprz).
The team found that while 10 out of 12 mice developed ulcers after being fed VacA, none of the mice lacking Ptprz did.
VacA was still able to get inside stomach cells (probably via other receptors), but without Ptprz it could not transmit its toxic signals for causing ulcers.
In a related News and Views article, Dr Richard Peek comments that identifying proteins that mediate H. pylori infection and disease could lead to a vaccine against stomach ulcers.