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Bacterial infections in blood are often accompanied by blood coagulation, but this phenomenon has been believed to result from immune and inflammatory responses. Rustem F. Ismagilov of the University of Chicago and coworkers now show that the bacteria themselves can trigger coagulation under the right circumstances (Nat. Chem. Biol., DOI: 10.1038/nchembio.124). The researchers found that activation of blood coagulation depends on the clustering of bacterial cells rather than on the total amount of bacteria present. For example, coagulation occurs quickly when bacteria are bunched but not at all when they are widely dispersed. When triggering coagulation, the bacteria bypassed the normal initiation points of coagulation pathways, which involve coagulation factors VII and XII, and instead directly activated prothrombin (factor II) and factor X. In the case of Bacillus anthracis, the researchers found that this coagulation pathway requires the zinc metalloprotease InhA1. Ismagilov and coworkers refer to the mechanism used by the bacteria as "quorum acting" because it involves secreting a molecule that exerts an effect on the environment only after the bacteria reach a sufficient local density.
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