Helicobacter pylori modulates host cell responses by CagT4SS-dependent translocation of an intermediate metabolite of LPS inner core heptose biosynthesis

@inproceedings{Stein2017HelicobacterPM,
  title={Helicobacter pylori modulates host cell responses by CagT4SS-dependent translocation of an intermediate metabolite of LPS inner core heptose biosynthesis},
  author={Saskia C Stein and Eugenia Faber and Simon H. Bats and Tatiana Murillo and Yvonne Speidel and Nina Coombs and Christine Josenhans},
  booktitle={PLoS pathogens},
  year={2017}
}
Highly virulent Helicobacter pylori cause proinflammatory signaling inducing the transcriptional activation and secretion of cytokines such as IL-8 in epithelial cells. Responsible in part for this signaling is the cag pathogenicity island (cagPAI) that codetermines the risk for pathological sequelae of an H. pylori infection such as gastric cancer. The Cag type IV secretion system (CagT4SS), encoded on the cagPAI, can translocate various molecules into cells, the effector protein CagA… CONTINUE READING