Helicobacter pylori BabA-SabA Key Roles in the Adherence Phase: The Synergic Mechanism for Successful Colonization and Disease Development

Abstract

Helicobacter pylori is a pathogenic microorganism that successfully inhabits the human stomach, colonizing it by producing several virulence factors responsible for preventing host self-defense mechanisms. The adherence mechanism to gastric mucosal tissue is one of the most important processes for effective colonization in the stomach. The blood group antigen-binding adhesion (BabA) and sialic acid-binding adherence (SabA) are two H. pylori outer membrane proteins able to interact with antigens in the gastroduodenal tract. H. pylori possesses several mechanisms to control the regulation of both BabA and SabA in either the transcriptional or translational level. BabA is believed to be the most important protein in the early infection phase due to its ability to interact with various Lewis antigens, whereas SabA interaction with sialylated Lewis antigens may prove important for the adherence process in the inflamed gastric mucosal tissue in the ongoing-infection phase. The adherence mechanisms of BabA and SabA allow H. pylori to anchor in the gastric mucosa and begin the colonization process.

Keywords: BabA; SabA; adherence; infectious disease.

Figure 1

Schematic of H. pylori’s anchoring processes facilitated by BabA and SabA. (A) In a healthy gastric epithelium cell, BabA can bind with various antigens, such as the A/B-Le^b, MUC5AC, MUC1, and H type 1 antigen. The ability of BabA to interact with various antigens shows its importance in the initial adherence process on the gastric epithelial cells. (B) sLe^x and sLe^a antigens are upregulated in inflamed gastric epithelium cells. Therefore, SabA might play a more important role for anchoring to epithelium cells with an ongoing inflammation process.