Author:
Bugaytsova Jeanna A.,Moonens Kristof,Piddubnyi Artem,Schmidt Alexej,Edlund Johan Olofsson,Lisiutin Gennadii,Brännström Kristoffer,Chernov Yevgen A.,Thorel Kaisa,Tkachenko Iryna,Sharova Oleksandra,Vikhrova Iryna,Butsyk Anna,Shubin Pavlo,Chyzhma Ruslana,Johansson Daniel X.,Marcotte Harold,Sjöström Rolf,Shevtsova Anna,Bylund Göran,Rakhimova Lena,Lundquist Anders,Berhilevych Oleksandra,Kasianchuk Victoria,Loboda Andrii,Ivanytsia Volodymyr,Hultenby Kjell,Persson Mats A. A.,Gomes Joana,Matos Rita,Gartner Fátima,Reis Celso A.,Whitmire Jeannette M.,Merrell D. Scott,Pan-Hammarström Qiang,Landström Maréne,Oscarson Stefan,D’Elios Mario M.,Agreus Lars,Ronkainen Jukka,Aro Pertti,Engstrand Lars,Graham David Y.,Kachkovska Vladyslava,Mukhopadhyay Asish,Chaudhuri Sujit,Karmakar Bipul Chandra,Paul Sangita,Kravets Oleksandr,Camorlinga Margarita,Torres Javier,Berg Douglas E.,Moskalenko Roman,Haas Rainer,Remaut Han,Hammarström Lennart,Borén Thomas
Abstract
SUMMARYThe majority of the world population carry the gastric pathogenHelicobacter pylori. Fortunately, most individuals experience only low-grade or no symptoms, but in many cases the chronic inflammatory infection develops into severe gastric disease, including duodenal ulcer disease and gastric cancer. Here we report on a protective mechanism whereH. pyloriattachment and accompanying chronic mucosal inflammation can be reduced by antibodies that are present in a vast majority ofH. pyloricarriers. These antibodies block binding of theH. pyloriattachment protein BabA by mimicking BabA’s binding to the ABO blood group glycans in the gastric mucosa. However, many individuals demonstrate low titers of BabA blocking antibodies, which is associated with an increased risk for duodenal ulceration, suggesting a role for these antibodies in preventing gastric disease.
Publisher
Cold Spring Harbor Laboratory