Description:
<jats:title>Abstract</jats:title>
<jats:p>Trypanosoma cruzi is an intracellular obligate parasite and the causative agent of Chagas disease. Previous work has shown that the chemokine receptor CCR5 plays a role in systemic responses against T. cruzi. We evaluated whether CCR5 plays a critical role in mucosal protection against natural oral and conjunctival challenges. Memory-immune CCR5-/- and wild-type C57BL/6 mice were generated by repeated infectious challenges with sublethal doses of insect-derived metacyclic trypomastigotes. Similar IgA, IgG and IFN-γ responses were detected in the spleen in both memory-immune and primary infected wild-type and CCR5-/- mice. More importantly, protection was evaluated in memory-immune mice via real-time PCR and limiting dilution assay for parasite outgrowth. CCR5-/- memory-immune mice developed equivalent levels of protection against both oral and conjunctival mucosal challenges. Preliminary studies from the stomachs of CCR5-/- memory-immune mice showed an increase in the transcript levels of CCL5 as compared to memory-immune wild-type mice. Overall, it appears that CCR5 does not play a critical role in the control of parasite replication and immune responses at sites of initial mucosal infection with T. cruzi. However, CCL5 signaling through CCR1 and/or CCR3 may compensate for the absence of CCR5.</jats:p>