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.

Figure 1*T. cruzi* (blue dots) thrives in cells lacking (bottom) TXA~2~ receptors.

*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 (TXA~2~). When produced by human cells, TXA~2~ has pro-inflammatory effects and can cause cardiac injury by triggering platelet aggregation, clotting, and vasoconstriction.

The parasitic TXA~2~ 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 TXA~2~ 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 TXA~2~ receptor. The group is now dissecting TXA~2~ 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 TXA~2~ 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. ![](jem_iti_end.jpg)

[^1]: <hbashyam@rockefeller.edu>
