This study was led by Dr Le Son Tran and A/Prof Richard Ferrero
The bacterium Helicobacter pylori (H. pylori) infects half of the world’s population and is the main cause of gastric cancer. To establish its long-term colonization in the stomach, this bacterium has developed several strategies to dampen the host immune response. In this study, we have unravelled a part of that mystery, identifying an immune sensor, NOD1, which triggers the secretion of an immune suppressor protein, called interleukin-33 (IL-33), in response to H. pylori infection.
Centre for Innate Immunity & Infectious Diseases
Gastrointestinal Infection and Inflammation
Journal and article title
NOD1 has previously been known to be a protein required for protection against H. pylori infection. However, we demonstrated for the first time that NOD1 signalling can be hijacked by H. pylori to dampen host immune responses.
Our results provide the rationale for future studies examining whether targeting this immunological pathway could prevent bacterial persistence and reduce cancer risk.
Gastric cancer, Helicobacter pylori infection
Other points of interest
In this study, we have successfully applied technologies, such as multiplex ELISA and CRISPR/Cas9, to study the mechanisms underlying host-pathogen interactions, which may be of interest to researchers at the Hudson Institute.