Researchers at Baylor College of Medicine and collaborating institutions have discovered a mechanism that drives the long-term decline in immune response that is observed after tuberculosis (TB) has been successfully treated. Their findings, published in the Proceedings of the National Academy of Sciences , suggest a potential new way to restore immune responsiveness and reduce mortality risk after severe infections. "Sepsis and TB are associated with loss of protective immune responses and increased mortality post successful treatment," said Dr.
Andrew DiNardo, corresponding author and associate professor in the section of infectious diseases and division of pediatric global and immigrant health at Baylor College of Medicine and Texas Children's Hospital. "In the current study, we investigated what mediated the perturbation of immune function after severe infections." Researchers know that severe and chronic infections in humans and animals result in persistent, long-lasting epigenetic changes.
These changes refer to alterations in chemical markings on the DNA that tell cells in the body which genes to turn on or off. For instance, TB dampens immune responsiveness by adding extra methyl chemical tags (DNA methylation) to certain genes involved in immune responses. In turn, this results in decreased production of proteins mediating immune defense and increased susceptibility to infections.
However, the mechanisms inducing epigenetic changes in infections were not clear. Previ.