Chlamydia as an obligate intracellular pathogen with only limited coding capacity entirely depends on the uptake of metabolites from the host cell. The continuous consumption of metabolites from the host automatically results in a conflict between the fast replicating bacteria and the cell for nutrient resources. In addition, Chlamydia infection causes severe stress to the host which may result in the induction of host cell death and loss of the only nutrient resources of these bacteria. In this project we aim to understand how Chlamydia access different nutrient pools in severely stressed host cells. Our data indicate that downregulation of the tumour suppressor protein p53 is central to both, counteracting stress responses and unleashing nutrient pools from the host cell. Protection of mitochondrial integrity is thereby a central strategy to secure high ATP levels as an energy source for the rapidly dividing Chlamydia.