| First Author | Hardison JL | Year | 2006 |
| Journal | J Infect Dis | Volume | 193 |
| Issue | 11 | Pages | 1584-8 |
| PubMed ID | 16652288 | Mgi Jnum | J:144907 |
| Mgi Id | MGI:3832158 | Doi | 10.1086/503812 |
| Citation | Hardison JL, et al. (2006) Chemokine CC receptor 2 is important for acute control of cardiac parasitism but does not contribute to cardiac inflammation after infection with Trypanosoma cruzi. J Infect Dis 193(11):1584-8 |
| abstractText | 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. |
