Editorial
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Jul 21, 2008; 14(27): 4265-4272
Published online Jul 21, 2008. doi: 10.3748/wjg.14.4265
Roles of Helicobacter pylori BabA in gastroduodenal pathogenesis
Yoshio Yamaoka
Yoshio Yamaoka, Department of Medicine-Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas 77030, United States
Author contributions: Yamaoka Y designed and wrote the paper.
Correspondence to: Yoshio Yamaoka, MD, PhD, Department of Medicine, Michael E. DeBakey Veterans Affairs Medical Center 2002 Holcombe Blvd. (111D) Rm 3A-320, Houston, Texas 77030, United States. yyamaoka@bcm.tmc.edu
Telephone: +1-713-7947597
Fax: +1-713-7954471
Received: February 28, 2008
Revised: May 4, 2008
Accepted: May 11, 2008
Published online: July 21, 2008
Abstract

Interactions between BabA and Lewis b (Leb) related antigens are the best characterized adhesin-receptor interactions in Helicobacter pylori (H pylori). Several mechanisms for the regulation of BabA expression are predicted, including at both transcriptional and translational levels. The formation of chimeric proteins (babA/B or babB/A chimeras) seems to play an especially important role in translational regulation. Chimeric BabB/A protein had the potential to bind Leb; however, protein production was subject to phase variation through slipped strand mispairing. The babA gene was cloned initially from strain CCUG17875, which contains a silent babA1 gene and an expressed babA2 gene. The sequence of these two genes differs only by the presence of a 10 bp deletion in the signal peptide sequence of babA1 that eliminates its translational initiation codon. However, the babA1 type deletion was found only in strain CCUG17875. A few studies evaluated BabA status by immunoblot and confirmed that BabA-positive status in Western strains was closely associated with severe clinical outcomes. BabA-positive status also was associated with the presence of other virulence factors (e.g. cagA-positive status and vacA s1 genotype). A small class of strains produced low levels of the BabA protein and lacked Leb binding activity. These were more likely to be associated with increased mucosal inflammation and severe clinical outcomes than BabA-positive strains that exhibited Leb binding activity. The underlying mechanism is unclear, and further studies will be necessary to investigate how the complex BabA-receptor network is functionally coordinated during the interaction of H pylori with the gastric mucosa.

Keywords: Helicobacter pylori; BabA; Pathogenesis; Lewis antigens