“Organisms that promote dysbiosis (a compositional shift in the microbiota), such as the bacterium Porphyromonas gingivalis, are faced with a conun- drum: on the one hand, they need to evade immune-mediated killing but on the other hand, they require inflammation, as this produces the nutrients that they need to survive through tissue breakdown. In a new study, Hajishengallis and colleagues reveal how P. gingivalis manipulates host neutrophils to solve this problem. P. gingivalis is a pathogen of the oral cavity, a location in which neutrophils are known to act as the main phagocytes. Because the bacterium requires intact signalling through complement C5a receptor (C5AR; also known as C5AR1) to drive dysbiosis, and because it is recognized by Toll-like receptor 2 (TLR2), the authors postulated that P. gingivalis exploits these pathways in neutrophils to avoid killing yet promote periodontal inflammation.”

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