Inflammasome activation and regulation during Helicobacter pylori pathogenesis

Helicobacter pylori is a leading cause of gastric cancer worldwide, its type four secretary toxin CagA is cited to be primarily responsible for it. Other virulence factors such as urease, VacA, HopQ, BabA and SabA are responsible for bacterial survival in acidic environment, adherence and cellular damage but its molecular mechanism is not completely understood. A number of pathogens including bacteria, fungi and virus are involved in the regulation of cellular machinery of inflammasome. Inflammasomes are multimeric protein complexes formed after external stimuli such as PAMPs/DAMPs or salt crystals and activates cellular caspases causes inflammation via pro-inflammatory cytokines. Virulence factors associated with microbial pathogens causes’ cellular damage through damaging mitochondria, rupturing lysosome, producing endoplasmic stress and dysregulation of cellular ions balance. These cellular dysfunctioning leads to oxidative stress, cathepsin B production, nuclear and mitochondrial DNA damage which activates inflammasome machinery, pro-inflammatory cytokine release and cellular death known as pyroptosis. The mechanism of inflammasome induction by H. pylori is not studied extensively and very few virulence factors such as UreB, CagA, FlaA and VacA and their role in inflammasomes is established. This review elaborates the mechanism of inflammasomes regulation and elucidates the pathways through which H. pylori regulates inflammasome activation.