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Helicobacter pylori Adapts to Chronic Infection and Gastric Disease via pH-Responsive BabA-Mediated Adherence

Research output: Contribution to journalArticle

Jeanna A Bugaytsova, Oscar Björnham, Yevgen A Chernov, Pär Gideonsson, Sara Henriksson, Melissa Mendez, Rolf Sjöström, Jafar Mahdavi, Anna Shevtsova, Dag Ilver, Kristof Moonens, Macarena P Quintana-Hayashi, Roman Moskalenko, Christopher Aisenbrey, Göran Bylund, Alexej Schmidt, Anna Åberg, Kristoffer Brännström, Verena Königer, Susanne Vikström & 41 more Lena Rakhimova, Anders Hofer, Johan Ögren, Hui Liu, Matthew D Goldman, Jeannette M Whitmire, Jörgen Ådén, Justine Younson, Charles G Kelly, Robert H Gilman, Abhijit Chowdhury, Asish K Mukhopadhyay, G Balakrish Nair, Konstantinos S Papadakos, Beatriz Martinez-Gonzalez, Dionyssios N Sgouras, Lars Engstrand, Magnus Unemo, Dan Danielsson, Sebastian Suerbaum, Stefan Oscarson, Ludmilla A Morozova-Roche, Anders Olofsson, Gerhard Gröbner, Jan Holgersson, Anders Esberg, Nicklas Strömberg, Maréne Landström, Angela M Eldridge, Brett A Chromy, Lori M Hansen, Jay V Solnick, Sara K Lindén, Rainer Haas, Andre Dubois, D Scott Merrell, Staffan Schedin, Han Remaut, Anna Arnqvist, Douglas E Berg, Thomas Borén

Original languageEnglish
Pages (from-to)376-389
Number of pages14
JournalCell Host & Microbe
Volume21
Issue number3
Early online date8 Mar 2017
DOIs
Publication statusE-pub ahead of print - 8 Mar 2017

King's Authors

Abstract

The BabA adhesin mediates high-affinity binding of Helicobacter pylori to the ABO blood group antigen-glycosylated gastric mucosa. Here we show that BabA is acid responsive-binding is reduced at low pH and restored by acid neutralization. Acid responsiveness differs among strains; often correlates with different intragastric regions and evolves during chronic infection and disease progression; and depends on pH sensor sequences in BabA and on pH reversible formation of high-affinity binding BabA multimers. We 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 and that bio-selection 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. These processes generate diverse H. pylori subpopulations, in which BabA's adaptive evolution contributes to H. pylori persistence and overt gastric disease.

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