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Access through your institution Buy or subscribe _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. Using an _in vivo_ model that allows the quantitative assessment
of bacterium–neutrophil interactions, they found that _C5ar__−/−_ or _Tlr2__−/−_ mice had reduced numbers of viable _P. gingivalis_. The inhibition or loss of either C5AR or TLR2 had the
same effect on _P. gingivalis_ survival, suggesting that these receptors probably engage in cooperative crosstalk to prevent bacterial killing. Similar findings were obtained using human
neutrophils _in vitro_. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive 12 print
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local taxes which are calculated during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES *
Maekawa, T. et al. _Porphyromonas gingivalis_ manipulates complement and TLR signaling to uncouple bacterial clearance from inflammation and promote dysbiosis. _Cell Host Microbe_ 15,
768–778 (2014) Article CAS PubMed PubMed Central Google Scholar Download references Authors * Rachel David View author publications You can also search for this author inPubMed Google
Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE David, R. Two routes to success. _Nat Rev Immunol_ 14, 519 (2014).
https://doi.org/10.1038/nri3723 Download citation * Published: 18 July 2014 * Issue Date: August 2014 * DOI: https://doi.org/10.1038/nri3723 SHARE THIS ARTICLE Anyone you share the following
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