Porphyromonas gingivalis – little bugger makes big disease states!

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        Here are a few articles on yet another gram-negative bacteria that causes many nasty, chronic health conditions in us humans. This one is well known by dental professionals.

        Federation of American Societies for Experimental Biology
        Smile: Gingivitis bacteria manipulate your immune system so they can thrive in your gums

        New research published in the Journal of Leukocyte Biology suggests that Porphyromonas gingivalis causes excess IL-10 production, which inhibits the immune cells interferon gamma leading to infection

        A new research report published in the Journal of Leukocyte Biology shows how the bacteria known for causing gum disease–Porphyromonas gingivalis–manipulates the body’s immune system to disable normal processes that would otherwise destroy it. Specifically, the report shows that this pathogen prompts the production of the anti-inflammatory molecule Interleukin-10 (IL-10). This, in turn, inhibits the function of T-cells, which would otherwise help to protect the host from this particular microbial infection.

        “Since greater than 50 percent of the U.S. population over 50 years-of-age develop adult periodontal disease, we hope that the results of our study will ultimately help in the development of novel treatments that could prevent or ameliorate the chronic infection caused by the pathogen P. gingivalis,'” said Jannet Katz, D.D.S., Ph.D., a researcher involved in the work from the Department of Pediatric Dentistry at the University of Alabama in Birmingham.

        To make this discovery, scientists used cells from mice that were exposed to P. gingivalis. One portion of the cells was treated with an inhibiting antibody against IL-10 and the other portion of cells was not treated. All of the cells were then tested for interferon gamma production. An increase of interferon gamma production was seen in the treated cells, but no increase was found in the untreated cells. These findings suggest that the damage done by P. gingivalis happens when the immune cells of the host are first exposed to this pathogen, and further implies that for treatment to be successful, it must be started as early as possible. This study highlights the mechanism by which P. gingivalis can establish a chronic infection in the form of periodontal disease and provides insight into how the disease develops. Results also demonstrate the importance of very early intervention either by eradication of the bacterium with specifically designed therapeutics or by prevention via the development of an effective vaccine.

        “Gum diseases and the infections that cause them can be incredibly stubborn and difficult to treat,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. “What isn’t as well known is why these infections are so difficult to eradicate. These new studies now demonstrate that these bacteria go beyond merely evading our body’s defenses and actually manipulate our immune systems for their own survival.”


        The Journal of Leukocyte Biology publishes peer-reviewed manuscripts on original investigations focusing on the cellular and molecular biology of leukocytes and on the origins, the developmental biology, biochemistry and functions of granulocytes, lymphocytes, mononuclear phagocytes and other cells involved in host defense and inflammation. The Journal of Leukocyte Biology is published by the Society for Leukocyte Biology.

        Dalia E. Gaddis, Craig L. Maynard, Casey T. Weaver, Suzanne M. Michalek, and Jannet Katz. Role of TLR2-dependent IL-10 production in the inhibition of the initial IFN-γ T cell response to Porphyromonas gingivalis. J. Leukoc. Biol. January 2013 93:21-31; doi:10.1189/jlb.0512220 ; Role of TLR2-dependent IL-10 production in the inhibition of the initial IFN-.

        Contact: Cody Mooneyhan

        Source article:

        Role of TLR2-dependent IL-10 production in the inhibition of the initial IFN-γ T cell response to Porphyromonas gingivalis

        Dalia E. Gaddis*,1, Craig L. Maynard†, Casey T. Weaver†, Suzanne M. Michalek* and Jannet Katz‡,2
        + Author Affiliations

        Departments of *Microbiology,†Pathology, and ‡Pediatric Dentistry, University of Alabama at Birmingham, Birmingham, AL 35294-2170, USA

        Current address: Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.

        Correspondence: Dept. of Pediatric Dentistry, University of Alabama at Birmingham, 845 19th Street South, BBRB 258/5, Birmingham, AL 35294-2170, USA. E-mail: meow(at)uab.edu


        P.g., a Gram-negative bacterium, is one of the main etiological agents of the chronic inflammatory disease, periodontitis. Disease progression is thought to occur as a result of an inadequate immune response, which although happens locally, can also occur distally as a result of the dissemination of P.g. into the circulation. As IL-10 and TLR2 are pivotal molecules in the immune response that P.g. elicits, we hypothesized that TLR2-mediated IL-10 production, following the initial systemic exposure to P.g., inhibits the IFN-γ T cell response. To address this hypothesis, mice were primed with P.g., and the types of cells producing IL-10 and the capacity of T cells to produce IFN-γ following blocking or neutralization of IL-10 were assessed. Our results showed that upon initial encounter with P.g., splenic T cells and CD11b+ cells produce IL-10, which when neutralized, resulted in a substantial increase in IFN-γ production by T cells. Furthermore, IL-10 production was dependent on TLR2/1 signaling, partly in response to the major surface protein, FimA of P.g. In addition, P.g. stimulation resulted in the up-regulation of PD-1 and its ligand PD-L1 on CD4 T cells and CD11b+ cells, respectively. Up-regulation of PD-1 was partially dependent on IL-10 but independent of TLR2 or FimA. These results highlight the role of IL-10 in inhibiting T cell responses to the initial systemic P.g. exposure and suggest multiple inhibitory mechanisms potentially used by P.g. to evade the host’s immune response, thus allowing its persistence in the host.

        Porphyromonas gingivalis:

        From Wikipedia, the free encyclopedia

        Porphyromonas gingivalis belongs to the phylum Bacteroidetes and is a non-motile, Gram-negative, rod-shaped, anaerobic pathogenic bacterium. It forms black colonies on blood agar.

        It is found in the oral cavity, where it is implicated in certain forms of periodontal disease,[1] as well as the upper gastrointestinal tract, respiratory tract, and in the colon. Collagen degradation that is observed in chronic periodontal disease results in part from the collagenase enzymes of this species. It has been shown in an in vitro study by Irshad et al.[2] that P. gingivalis can invade human gingival fibroblasts and can survive inside in the presence of considerable concentrations of antibiotics. P. gingivalis also invades gingival epithelial cells in high numbers and both bacteria and epithelial cells survive for extended periods. In patients harbouring P. gingivalis one finds high levels of specific antibody in the serum.

        Additionally P. gingivalis has been linked to rheumatoid arthritis. P. gingivalis contains the PAD (Peptidyl-Arginine Deaminase) which is involved in citrullination.[3] Patients with Rheumatoid Arthritis have an increased incidence of periodontal disease and antibodies to the bacterium are significantly more common in patients with rheumatoid arthritis.[4]

        P. gingivalis is divided into K-serotypes based upon capsular antigenicity of the various types.[5]

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