The sexually transmitted disease Chlamydia is caused by the bacterium Chlamydia trachomatis, which infects human cells. In women, the infection can lead to pelvic inflammatory disease, and in men inflammation of the urethra is most common. Chlamydia can be spread during vaginal, anal, or oral sex, and can be passed from an infected mother to her baby during childbirth. Untreated, chlamydia infection can cause fallopian tubes blockage in women which can result in tubal pregnancy or infertility. Treatment is by antibiotics, such as azithromycin, erythromycin and ofloxacin. There are around 89 million cases around the world reported each year.
One concern with combating infections is in understanding how the bacterium survives in human cells. In a breakthrough, University of Würzburg (northern Bavaria, Germany) microbiologists have discovered that the bacterial pathogens can manipulate the energy suppliers of human cells in the invading process.
When Chlamydia trachomatis infects a human cell it needs to prevent the cell from triggering programmed cell death. If the cell dies, it sops the bacteria from replicating and therefore from spreading throughout the body. The invasive organism is also dependent upon the human cells to provide the necessary nutrients for survival.
The University of Würzburg scientists have discovered the mechanism by which Chlamydia trachomatis influences the mitochondria in the body cells. Mitochondria are the cells’ power plants and by controlling these the bacteria prevent the cells from dying. This find also opens the door to a new way of fighting the infection.
According to lead researcher Professor Thomas Rudel chlamydiae disable a tumour suppressor protein called p53 in infected cells. This triggers a process which repairs DNA damages, which arises from the chlamydia infection. The researchers think that by keep the p53 protein active the cells can destroy the bacteria.
The research has been published in The Journal of Cell Biology, under the heading “Chlamydia preserves the mitochondrial network necessary for replication via microRNA-dependent inhibition of fission.”
