Gingivitis bacteria found to manipulate immune system

October 23, 2014

BIRMINGHAM, Ala., USA: New research from the U.S. provides evidence that Porphyromonas gingivalis, the main agent of the chronic inflammatory disease periodontitis, also manipulates the human immune system. In a number of laboratory tests, scientists observed that the pathogen inhibits the body’s defense processes that would normally destroy it. In order to determine the manner in which P. gingivalis influences the immune system, the researchers treated cells from mice with an inhibiting antibody against Interleukin-10 (IL-10), an anti-inflammatory protein, while leaving a different portion of the same cells untreated. Afterwards, they tested whether the cells produced interferon-gamma (IFN-γ), a protein that has an immunostimulatory and antiviral effect. According to the study, P. gingivalis stimulated the production of IL-10, which in turn inhibited the activity of T-cells and macrophages, and repressed the immune response. The researchers observed increased production of IFN-γ in the treated cells, while no such growth was seen in the untreated cells. The study highlighted the mechanism by which the pathogen establishes a chronic infection. “These bacteria go beyond merely evading our body’s defense and actually manipulate our immune system for their own survival,” the researchers said. The findings suggested that the damage done by the bacterium occurs when the immune cells of the host are first exposed to the pathogen. With regard to successful treatment, the results demonstrated the importance of a very early intervention. According to the Centers for Disease Control and Prevention, one out of every two American adults aged over 30 have periodontitis. As the disease is often difficult to treat, the researchers hope that the findings of the current study will promote the development of new treatments that could prevent or ameliorate the chronic infections caused by the pathogen. The study was carried out at the University of Alabama at Birmingham’s School of Dentistry and was published in the January issue of the Journal of Leukocyte Biology.