Pathogenesis and clinical management of Helicobacter pylori gastric infection

Table 1  H. pylori adhesion molecules

Adhesin	Functions	Ref.
BabA	Specific binding to the b and H-1 Lewis antigens from the surface of the gastric epithelial cells	[105]
SabA	Binding to Lex, which is upregulated in gastric epithelial cells by H. pylori after initial colonization mediated by BabA. Also allows the adherence of the bacterium to laminin, an extracellular matrix protein	[106,107]
AlpA and AlpB	Mediation of adherence to gastric mucosal cells and promotion of inflammatory intracellular signaling cascades (might induce IL-8 and IL-6)	[108]
OipA	Adhesion to the gastric mucosa cells and promotion of proinflammatory environment (associated with IL-8 increase, mucosal damage and duodenal ulcer)	[109]
HopQ	Interaction with CEACAM family proteins of gastric mucosal cells, allowing CagA translocation. Might inhibits the activity of natural killer cells and T cells	[110]
HopZ	Interaction with undeterm ined receptors, promoting adhesion to gastric cells	[111]

H. pylori: Helicobacter pylori; CagA: Cytotoxin associated antigen A; IL: Interleukin; BabA: Binding adhesin A; OipA: Outer inflammatory protein.