Research ArticleHost-Pathogen Interactions

Microbial Hijacking of Complement–Toll-Like Receptor Crosstalk

See allHide authors and affiliations

Science Signaling  16 Feb 2010:
Vol. 3, Issue 109, pp. ra11
DOI: 10.1126/scisignal.2000697

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Disarming Crosstalk

The complement system is a key antimicrobial defense system and consists of a set of serum proteins that are converted to their active form by proteolytic cleavage. Many pathogens try to disable the complement system as part of their infection strategy. However, Porphyromonas gingivalis, an oral pathogen implicated in periodontitis and atherosclerosis, generates C5a, which is one of the active fragments of the fifth complement component and a macrophage chemoattractant. Wang et al. show that P. gingivalis evades the innate immune system by subverting communication between the C5a receptor (C5aR) and Toll-like receptor 2 (TLR2), another receptor that normally initiates antimicrobial responses. P. gingivalis and C5a combined to increase intracellular concentrations of cyclic adenosine monophosphate (cAMP), which suppressed macrophage function, and decrease production of nitric oxide, which enhanced P. gingivalis survival. These effects required crosstalk and association between C5aR and TLR2. Blockade of C5aR prevented the ability of P. gingivalis to evade the innate immune system and thus may be a therapeutic strategy in diseases involving this pathogen.

View Full Text

Stay Connected to Science Signaling