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T. cruzi (blue dots) thrives in cells lacking (bottom) TXA2 receptors.
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On page 929, Ashton et al. report that an intracellular parasite regulates its own growth and exploits the inflammatory environment within its host to continue its survival and mediate long-term damage.
Trypanosoma cruzi, the bug that causes Chagas' disease, initiates a short-lived acute infection in humans. A third of those infected, however, develop chronic cardiac disease that sets in after a long asymptomatic period. The mechanism by which the parasite facilitates this long-term pathology is still unclear.
Ashton et al. now show that the parasite infects vascular endothelial cells and secretes a bioactive lipid called thromboxane (TXA2). When produced by human cells, TXA2 has pro-inflammatory effects and can cause cardiac injury by triggering platelet aggregation, clotting, and vasoconstriction.
The parasitic TXA2 also promotes cardiac injury, the team finds, yet it somehow mediates an anti-inflammatory immune response in the host. Mice that lack cell surface receptors for TXA2 had increased inflammatory damage.
These mice also had a higher parasite load than wild-type mice, suggesting that the parasite suppresses its own replication by a negative feedback through the TXA2 receptor. The group is now dissecting TXA2 receptor signaling within infected cells to determine how the parasite controls its own growth rate.
The team speculates that, within infected cells, the parasite uses TXA2 to limit its own growth and minimize cell damage, thus ensuring its survival. But parasite-secreted TXA2 also engages receptors on uninfected host cells, which might eventually cause the heart disease seen in chronic infections. 
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