Roles of the BabA and the SabA adhesins in gastroduodenal diseases

Abstract

Adhesion is an important prerequisite for colonization and it is the initial step in infections with pathogenic bacteria. Adherence to host epithelial surfaces is the result of bacterial surface proteins, called adhesins, and their specific interaction with cognate protein- or glycoconjugate receptors on the host cells. Often, the bacteria have a set of complementary adhesins that are specific for different host receptors. Alternative mechanism has been suggested to mediate H. pylori adhesion, and this chapter will focus on the two well-characterized adhesins BabA and SabA. In the healthy gastric mucosa, the Lewis b antigen (Leb) is present in the gastric epithelial lining of blood group O (H-antigen), B, and A individuals. H. pylori binding to ABO/Leb is mediated by the blood group antigen-binding BabA adhesin. As the inflammation develops, Leb is downregulated and the levels of sialylated antigens increase. Sialyl-Lewis x/a antigens (sLex/a) are specifically recognized by the H. pylori sialic acid-binding adhesin SabA. Even though bacterial adherence per se cannot cause disease, adherence is considered as a crucial step in pathogenesis since it is needed for bacterial delivery of effector molecules into the host cell. The presence of receptors and host-immune responses are two factors that differently affect adhesion. To achieve long-term colonization, H. pylori must regulate the expression of a cognate adhesin to fit the available receptors. Adhesion to the gastric epithelial cells promotes gain of nutrients, but too tight adhesion may be intimidating because of the risk of clearance by the bacteria for life-threatening immune responses. Thus, expression levels of the adhesins must be fine-tuned in accord to host receptor expression levels. This chapter will also discuss H. pylori adhesion in relation to severe gastric diseases.