Back

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.

2023-05-24 immunology
10.1101/2023.05.24.542096 bioRxiv
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.

Matching journals

The top 5 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.