10 August 2017 - PRESS RELEASE

New approach to gastritis treatment

Scientists from the Hannover Medical School (MHH) have elucidated how Helicobacter pylori causes gastritis. Chronic infections with the globally ubiquitous pathogen can also lead to gastric ulcers and gastric cancer. The DZIF was involved in the study.


Dr Saskia C. Stein, Prof Christine Josenhans and Eugenia Faber (left to right)© MHH/Kaiser

Hope in the fight against cancer: 40 percent of all Germans and even 50 of the global population are colonised with Helicobacter pylori in the stomach. It is the main cause of chronic gastritis which can also lead to the development of gastric ulcers or cancer. Scientists from the Hannover Medical School (MHH) have now discovered one of the most important mechanisms employed by the bacteria: by means of a specific bacterial injection system it injects parts of its envelope into gastric mucosa cells. In the gastric mucosa, these encounter specific proteins which transmit infection signals to the cell nucleus. Professor Christine Josenhans’ research team from the Institute for Medical Microbiology and Hospital Epidemiology published the findings in the journal Plos Pathogens.

With the help of CRISPR-Cas9 genetic scissors, the researchers were also able to identify one of the proteins that transmits infection signals to the cell nucleus, a so-called adaptor protein called TIFA. “These findings will help develop new treatment approaches for this type of chronic gastritis, particularly also for the potential gastric cancer that could develop,” says Professor Josenhans. To date, Helicobacter pylori infections have mainly been treated with antibiotics.

The MHH team’s work was funded by the Collaborative Research Centre (SFB) 900 “Chronic Infections: Microbial Persistence and its Control” which is financed by German Research Foundation, as well as by the German Center for Infection Research (DZIF).

Prof Christine Josenhans
T +49 511 532-4348

Saskia C. Stein et al:
Helicobacter pylori modulates host cell responses by CAGT4SS-dependent translocation of an intermediate metabolite of LPS inner core heptose biosynthesis.

Plos Pathogens July 17, 2017
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