Staphylococcus aureus Lpl Lipoproteins Delay G2/M Phase Transition in HeLa Cells
In recent years, numerous bacterial pathogens have been shown to inactivate the major tumour suppressor p53 during infection. This inactivation impedes the protective response of the host cell to the genotoxicity that often results from bacterial infection. Moreover, a new aspect of the antibacterial activity of p53 that has recently come to light — downregulation of host cell metabolism to interfere with intracellular bacterial replication — has further highlighted the crucial role of p53 in host–pathogen interactions, as host cell metabolism is relevant for all intracellular bacteria, as well as other pathogens that replicate inside host cells and use host metabolites. In this Progress article, we summarize recent work that has advanced our knowledge of the interaction between pathogenic bacteria and p53, and we discuss the known and expected outcomes of this interaction for pathogenesis.