Update on molecular pathogenesis of Helicobacter pylori-induced gastric cancer

Table 2 Some other virulence factors involved in the pathogenicity of Helicobacter pylori infection

Virulence factors	Mechanisms of action
Lipopolysaccharide	Triggers several signaling pathways
	Induces several inflammatory responses
	Induces immune responses
	Disrupts the mucus secretion
	Shielding the organism against toxic materials
Phospholipase	Activates signaling pathways (e.g., ERK1/2)
	Trigger chronic inflammation
	Enhances bacterial colonization and survival
	Involved in the degradation of lipids and damage to the mucus layer
Heat shock proteins	Enhance adherence to epithelial surfaces
	Involved in urease activation
	Control apoptosis and autophagy
	Help to maintain the structure and properties of the effector proteins
	Protect the cell from reactive oxygen species (ROS)
	Induce the production and release of IL-8, TNF-α and COX-2
Arginase	Prevents bacterial killing
	Prevents T-cell proliferation
	Impair immune responses
	Stimulate apoptosis
	Help the H. pylori to withstand the acidic environment
Superoxide dismutase	Protects the cell from ROS
	Enhances colonization
	Inhibits the production of cytokines
	Stimulates macrophage activation
γ-glutamyl-transferase	Facilitates apoptosis and necrosis
	Induces the release of pro-inflammatory proteins
	Induces the release of ROS
	Stimulates DNA damage
Cholesteryl α-glucosyltransferase (αCgT)	Shields H. pylori from immunological attack
	Stimulates the production of pro-inflammatory proteins (e.g., IL-8)
	Enhances bacterial growth and its resistance to antibiotics

TNF-α: Tumor necrosis factor alpha; IL: Interleukin; Helicobacter pylori: H. pylori.