Helicobacter pylori attachment-blocking antibodies protect against duodenal ulcer disease
Boren, T.; Bugaytsova, J. A.; Moonens, K.; Piddubnyi, A.; Schmidt, A.; Edlund, J. O.; Lisiutin, G.; Brannstrom, K.; Chernov, Y. A.; Thorell, K.; Tkachenko, I.; Sharova, O.; Vikhrova, I.; Butsyk, A.; Shubin, P.; Chyzhma, R.; Johansson, D. X.; Marcotte, H.; Sjostrom, R.; Shevtsova, A.; Bylund, G.; Rakhimova, L.; Lundquist, A.; Berhilevych, O.; Kasianchuk, V.; Loboda, A.; Ivanytsia, V.; Hultenby, K.; Persson, M. A. A.; Gomes, J.; Matos, R.; Gartner, F.; Reis, C. A.; Whitmire, J. M.; Merrell, D. S.; Pan-Hammarstrom, Q.; Landstrom, M.; Oscarson, S.; DElios, M. M.; Agreus, L.; Ronkainen, J.; Aro, P.
Show abstract
The majority of the world population carry the gastric pathogen Helicobacter 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 where H. pylori attachment and accompanying chronic mucosal inflammation can be reduced by antibodies that are present in a vast majority of H. pylori carriers. These antibodies block binding of the H. pylori attachment protein BabA by mimicking BabAs 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.
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