VacA-induced
death of these cells is a caspase-independent process that results in cellular release of histone-binding
protein high mobility group box 1 (HMGB1), a proinflammatory protein. These features are consistent
with the occurrence of cell death through a programmed necrosis pathway and suggest that VacA can be
included among the growing number of bacterial pore-forming toxins that induce cell death through
programmed necrosis.