|Title||Helicobacter pylori Adapts to Chronic Infection and Gastric Disease via pH-Responsive BabA-Mediated Adherence.|
|Publication Type||Journal Article|
|Year of Publication||2017|
|Authors||Bugaytsova, J. A., O. Björnham, Y. A. Chernov, P. Gideonsson, S. Henriksson, M. Mendez, R. Sjöström, J. Mahdavi, A. Shevtsova, D. Ilver, K. Moonens, M. P. Quintana-Hayashi, R. Moskalenko, C. Aisenbrey, G. Bylund, A. Schmidt, A. Åberg, K. Brännström, V. Königer, S. Vikström, L. Rakhimova, A. Hofer, J. Ögren, H. Liu, M. D. Goldman, J. M. Whitmire, J. Ådén, J. Younson, C. G. Kelly, R. H. Gilman, A. Chowdhury, A. K. Mukhopadhyay, B. G Nair, K. S. Papadakos, B. Martinez-Gonzalez, D. N. Sgouras, L. Engstrand, M. Unemo, D. Danielsson, S. Suerbaum, S. Oscarson, L. A. Morozova-Roche, A. Olofsson, G. Gröbner, J. Holgersson, A. Esberg, N. Strömberg, M. Landström, A. M. Eldridge, B. A. Chromy, L. M. Hansen, J. V. Solnick, S. K. Lindén, R. Haas, A. Dubois, S. D Merrell, S. Schedin, H. Remaut, A. Arnqvist, D. E. Berg, and T. Borén|
|Journal||Cell Host Microbe|
|Date Published||2017 Mar 08|
|Keywords||Adhesins, Bacterial, Bacterial Adhesion, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Hydrogen-Ion Concentration|
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.
|Alternate Journal||Cell Host Microbe|
|PubMed Central ID||PMC5392239|
|Grant List||R01 AI070803 / AI / NIAID NIH HHS / United States |
P51 OD011107 / OD / NIH HHS / United States
R01 DK063041 / DK / NIDDK NIH HHS / United States
R01 CA082312 / CA / NCI NIH HHS / United States
R01 AI081037 / AI / NIAID NIH HHS / United States
Helicobacter pylori Adapts to Chronic Infection and Gastric Disease via pH-Responsive BabA-Mediated Adherence.