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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 withTrypanosoma cruzi
Author(s) -
Jenny L. Hardison,
William A. Kuziel,
Jerry E. Manning,
Thomas E. Lane
Publication year - 2006
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/503812
Subject(s) - trypanosoma cruzi , inflammation , parasitism , immunology , chemokine , chagas disease , biology , medicine , parasite hosting , ecology , host (biology) , world wide web , computer science
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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