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BONFÁ, G. The role of CCR5 in oral infection by Toxoplasma gondii. 2010. 78f. Dissertação de Mestrado Faculdade de Medicina de Ribeirão Preto FMRP/USP-SP. T. gondii is an obligate intracellular protozoan parasite which is the causative agent of toxoplasmosis. In experimental model, C57BL/6 mice orally infected with a high parasitic load develop serious intestinal lesions, whose injuries are similar to those observed in Inflammatory Bowel Disease. This inflammation is caused due to parasite invasion of intestinal epithelial cells that elicit a robust Th1 type immune response. Moreover, chemokines produced by intestinal epithelial cells are involved in the migration and activation of inflammatory cells. In particular, the chemokine receptor CCR5 is important for cell recruitment in some infections and is involved with the migration of various cells subsets such as dendritic cells, T cells and, in particular regulatory T cells. CCR5 may also be related to mechanisms independent of cell migration, in which the intracellular signaling and activation of NF-κB may lead to intensification of the immune response. The role of CCR5 has not been clear in the experimental oral T. gondii infection. Thus, wild type C57BL/6 mice and CCR5 littermates were infected with T. gondii by gavage and immune and biochemical parameters, were analyzed at day 8 after infection. The CCR5 mice showed to be highly susceptible to the parasite, with intense inflammatory infiltration in the ilea and regions of epithelial ulcerations in comparison with WT mice. Both strain of mice presented inflammatory foci scattered by parenchyma of the liver, however the CCR5 mice presented an extensive hepatocyte vacuolization with an excessive accumulation of lipids in the organ and elevated serum triglycerides and transaminases concentration. The parasite load was significantly higher on small intestine and liver samples of CCR5 in comparison with WT mice. There was also a minor migration of NK cells in the small intestine, as well as greater frequency of CD4 T cells in this organ and a lower IFN-γ and IL-12p40 levels in liver homogenate samples in the CCR5 mice compared with WT mice. Gene expression analysis revealed a reduction in the formation of transcripts for PPARα in mice deficient in CCR5, and when the animals were treated with Gemfibrozil, a PPARα agonist, there was an improvement in the level of vacuolization and reduced triglycerides. These data suggest that a CCR5-dependent cell migration is essential for the modulation of T. gondii-induced inflammatory response in the small intestine. In addition, hepatic integrity during T. gondii oral infection is compromised in the absence of CCR5, and the molecular mechanisms involved can be related to PPARα expression.

Papel de CCR5 na infecção oral por Toxoplasma gondii