Chlamydia live inside human cells and entirely depend on host metabolites for their survival and proliferation. The same time, infection creates enormous stress to the host cell which cumulates in e.g. severe damage of the host’s DNA. In this research project we aim to understand how the bacteria generate their intracellular niche in the host cell, acquire nutrients from the host and subvert host cell metabolic control mechanism.
We currently investigate the role of oncogenic signalling in the metabolic adaptation of Chlamydia. Our recent data demonstrated a central role of the tumour suppressor p53 in the control of Chlamydia infection. p53 is actively downregulated in cells infected with Chlamydia to overcome the suppression of host metabolism and particularly preserve the function of mitochondria, a main source of metabolites for Chlamydia (read more).