Neutrophils are involved in the initial steps of most responses to pathogens and are essential components of the innate
immune response. Due to the ability to produce and release various soluble mediators, neutrophils may participate in the
regulation of the inflammatory response. Little is known about the role of neutrophils during protozoan infections including
infection by Trypanosoma cruzi. In the present study we investigated the importance of inflammatory neutrophils on
macrophage activation and T. cruzi replication in vitro, in cells obtained from BALB/c mice and C57Bl/6 mice. Co-cultures of
BALB/c apoptotic or live neutrophils with infected peritoneal macrophages resulted in increased replication of the parasites
and in the production of TGF-b and PGE2. The treatment with anti-TGF-b neutralizing antibody and COX inhibitor blocked
the parasite replication in vitro. On the other hand, co-cultures of T. cruzi infected macrophages with live neutrophils
isolated from C57BL/6 mice resulted in decreased number of trypomastigotes in culture and increased production of TNF-a
and NO. The addition of anti-TNF-a neutralizing antibody or elastase inhibitor resulted in the abolishment of macrophage
microbicidal effect and increased parasite replication. Addition of elastase to infected macrophages reduced the replication
of the parasites, and on the other hand, addition of a selective inhibitor of iNOS increased parasite growth, suggesting the
role of NO in this system. Our findings reveal that neutrophils may regulate T. cruzi experimental infection and determine
susceptibility and resistance to infection
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