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  1. M H McLean, Education editor
  1. Correspondence to Dr M H McLean, Division of Applied Medicine, Aberdeen University, School of Medicine and Dentistry, Foresterhill, Aberdeen AB25 2ZD, UK; m.h.mclean{at}abdn.ac.uk

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Helicobacter pylori infection evades gastric acidity

Bugaytsova JA, Björnham O, Chernov YA, et al. Helicobacter pylori adapts to chronic infection and gastric disease via pH-responsive BabA-mediated adherence. Cell Host Microbe 2017;21:376–389.

Helicobacter pylori (HP) infects billions of people worldwide and is linked to both peptic ulcer disease and gastric cancer. HP colonises the gastric epithelium and its overlying mucus and is partially protected against luminal acidity by epithelial secretions, intrinsic urease production and chemotaxis. In addition, tight adherence to mucosal glycan receptors assists in protection from luminal acidity. Bacterial attachment to these receptors is mediated by adhesins (attachment proteins) including BabA, which binds with high affinity to ABO/Leb blood group antigens to persist in the stomach mucosa. A multiauthor study by Bugaytsova and colleagues has shown that BabA-mediated HP adherence is acid sensitive, fully reversed when acidity is decreased. This is controlled by BabA adhesin protein's pH sensors sequence changes which are selected during chronic infection and disease. Given the heterogeneous nature of the HP-infected stomach environment, HP infection develops bacterial subpopulations that are optimised for different gastric habitats. The authors propose that BabA’s extraordinary reversible acid responsiveness enables tight mucosal bacterial adherence while also allowing an effective escape from epithelial cells and mucus that are shed into the acidic bactericidal lumen. In addition, bioselection and changes in BabA-binding properties through mutation and recombination with babA-related genes are selected by differences among individuals and by changes in gastric acidity over time. The findings also suggest that BabA also adapts its adherence properties to long-term acid secretion inhibition therapy with potential redistribution of HP infection and ensuing gastritis, increasing the risk of corpus atrophy and gastric cancer.

Could statins reduce the risk of developing hepatocellular carcinoma?

Bakiri L, Hamacher R, Graña O, et al. Liver carcinogenesis by FOS-dependent inflammation and cholesterol dysregulation. J Exp Med 2017. doi:10.1084/jem.20160935.)

The risk of hepatocellular carcinoma (HCC) arising in …

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