Chlamydia trachomatis infections can cause mutations in their host DNA by overriding mechanisms through which that host prevents the unregulated growth of genetically damaged cells—a potential cause of ovarian cancer, researchers at the Max Planck Institute for Infection Biology in Berlin (MPIIB) have found.
MPIIB researchers Thomas F. Meyer, Ph.D., director of MPIIB’s molecular biology department, and postdocs Cindrilla Chumduri and Rajendra Kumar Gurumurthy discovered that Chlamydia manipulates the host cell mechanism to favor its growth, inducing on the genome and epigenome long-lasting effects increasingly implicated in the development of a range of cancers, notably cervical and ovarian.
A paper published by the researchers “constitutes one important mosaic piece, corroborating a potential link between female ascending Chlamydia infections and ovarian cancer in particular,” MPIIB said in a statement.
The researchers found increased levels of DNA breaks in Chlamydia–infected cells compared with normal cells, which either “commit suicide” or activate repair by special protein complexes, depending on the extent of damage.
The process, DNA damage response, reseals broken DNA strands, ensuring the sequence of the genetic code has not been changed. In Chlamydia-infected cells, however, the response was impaired, leading to error-prone repair of the DNA breaks, a potential cause of mutations. Despite their extensive DNA damage, cells infected by Chlamydia continued to proliferate, facilitated by additional pro-survival signals activated in the host cells by Chlamydia.
Researchers “believe that this could be the first step on the path to carcinogenesis of the infected cells, due to uncontrolled cell growth in the presence of accumulating DNA damage—the hallmark of cancer,” MPIIB added.
Identifying an originating infection follows successful preventive strategies employed against gastric cancer agent Helicobacter pylori and cervical cancer agent Human Papiloma Virus (HPV). Earlier this week, the U.S. Centers for Disease Control and Prevention said the rate of infection among girls ages 14 and 19 fell by more than half (56%), from 11.5% to 5.1%, for the four forms of HPV covered by the vaccines Cervarix and Gardasil—even though only one-third of those girls have been vaccinated with the full three-dose course.
“Chlamydia infection promotes host DNA damage and proliferation but impairs the DNA damage response” was published online in Cell Host & Microbe June 12.
