Researchers have recognized a brand new mechanism by which a key bacterium in periodontitis evades the immune system. The research reveals that the bacterium exploits the protein CD47 to suppress immune responses, permitting it to persist in infected tissues and contribute to systemic ailments. Blocking CD47 or its ligand, thrombospondin-1, might provide a novel technique for enhancing bacterial clearance and bettering periodontal and total well being.
A latest research led by Prof. Gabriel Nussbaum from the College of Dental Drugs on the Hebrew College of Jerusalem has uncovered a novel immune evasion mechanism utilized by Porphyromonas gingivalis (P. gingivalis), a key bacterial perpetrator behind periodontitis- a extreme gum an infection. The research, revealed in PNAS, sheds mild on how this pathogen manipulates the immune system to persist in infected oral tissues, rising dangers for systemic ailments like heart problems, Alzheimer’s, and most cancers.
The analysis group discovered that P. gingivalis exploits the integrin-associated protein CD47 to intrude with the physique’s immune response. CD47, generally known as a “do not eat me” sign in most cancers cells, performs an important function in defending P. gingivalis from being destroyed by immune cells. Moreover, the research revealed that the bacterium induces the manufacturing of thrombospondin-1 (TSP-1), a ligand that additional suppresses immune exercise, significantly neutrophil-mediated bacterial clearance.
Our findings counsel that P. gingivalis makes use of CD47 to hijack immune signaling pathways, successfully disabling the host’s capability to clear the an infection. This mechanism helps clarify why this bacterium thrives in inflammatory environments, resulting in persistent periodontitis and probably contributing to different systemic ailments.”
Prof. Gabriel Nussbaum, College of Dental Drugs, Hebrew College of Jerusalem
Utilizing each in vitro and in vivo fashions, the researchers demonstrated that blocking CD47 or TSP-1 considerably enhanced bacterial clearance by the immune system. Mice missing CD47 confirmed the next capability to remove P. gingivalis, suggesting that concentrating on this pathway might present a promising technique for treating periodontal illness.
“Present periodontal remedies give attention to decreasing bacterial load mechanically, however understanding how these micro organism evade immune responses opens new therapeutic potentialities,” Prof. Nussbaum added. “Focusing on CD47-TLR2 signaling or TSP-1 might signify a novel strategy to managing persistent infections linked to oral and systemic well being.”
Given the robust correlation between periodontitis and circumstances akin to heart problems and neurodegenerative problems, this discovery holds broad implications past dentistry. Future analysis will discover how these findings can translate into medical therapies geared toward bettering immune responses to persistent bacterial infections.
Supply:
Hebrew College of Jerusalem
Journal reference:
Angabo, A., et al. (2025) CD47 and thrombospondin-1 contribute to immune evasion by Porphyromonas gingivalis. PNAS. doi.org/10.1073/pnas.2405534121.
