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Chemokine CC receptor 2 is important for acute control of cardiac parasitism but does not contribute to cardiac inflammation after infection with Trypanosoma cruzi.

  • Author(s): Hardison, Jenny L
  • Kuziel, William A
  • Manning, Jerry E
  • Lane, Thomas E
  • et al.

Published Web Location

https://doi.org/10.1086/503812Creative Commons 'BY' version 4.0 license
Abstract

The CC chemokine ligand 2 (CCL2) and CC chemokine receptor 2 (CCR2) are expressed in the heart after infection with Trypanosoma cruzi, suggesting that they play an important role in host defense. Infection of CCR2-deficient (CCR2(-/-)) mice with T. cruzi resulted in increased cardiac parasitism, yet the severity of cardiac inflammation was not affected. In addition, expression of interferon- gamma and inducible NO synthase in the heart, which are associated with effective killing of trypomastigotes, was not affected in CCR2(-/-) mice. These observations reveal that CCR2 signaling plays a distinct role that is separate from that of influencing either chemotaxis or previously defined anti-trypomastigote mechanisms for the control of T. cruzi's replication in the heart.

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