The paper up for discussion on Tuesday 19th March, 8pm UK time is on Helicobacter and can be found here
Helicobacter pylori is a bacterium that colonizes the stomach of about half the world’s population, most of whom are asymptomatic. However, some strains of H. pylori express a bacterial secretion system, a sort of molecular syringe that injects a bacterial protein inside the gastric cells and causes inflammation that can lead to peptic ulcer disease or gastric cancer. One of the essential components of the H. pylori secretion system is CagY, which is unusual because it contains a series of repetitive amino acid motifs that are encoded by a very large number of direct DNA repeats. Here we have shown that DNA recombination in cagY changes the protein motif structure and alters the function of the secretion system turning it on or off. Using mouse and non-human primate models, we have demonstrated that CagY is a molecular switch that ‘‘tunes’’ the host inflammatory response, and likely contributes to persistent infection. Determining the mechanism by which CagY functions will enhance our understanding of the effects of H. pylori on human health, and could lead to novel applications for the modulation of host cell function.
1. Is the paper well written, easy to understand and follow?
2. CagY variants evade the hosts immune response, any thoughts?
3. Is inflammation advantageous?
4. Anything you would do differently?