Heartless is expressed in longitudinal glial cells and both FGFRs are important in embryonic CNS development

n vitro, but easily proliferates in peritoneal macrophages of susceptible hosts, such as mice. McCabe and Remington demonstrated that freshly cultured rat macrophages killed more than 90% of the T. gondii ingested and that the surviving T. gondii did not replicate when they were observed for up to 72 hrs after ingestion. However, the mechanism of rat macrophage resistance to T. gondii remains yet to be determined. When stimulated with Th1 cytokines or with microbederived products, mouse macrophages express the inducible nitric oxide synthase, which synthesizes large amounts of nitric oxide through oxidation of L-arginase. NO is known to be a major effector molecule in macrophage-mediated cytotoxicity and therefore the macrophage-derived NO has been considered a key component of its defense against microbial agents, including Toxoplasma. Interestingly, T. gondii can easily infect and proliferate in mouse macrophages and reduce their ” NO production. Arginase shares the same substrate with iNOS. Two isoforms of arginase have been identified from macrophages of rat and mouse. Cytoplasmic arginase I and mitochondrial arginase II catalyze the same reaction. Arginase hydrolyzes Larginine to L-ornithine and urea. L-ornithine favors parasite Mechanism of Rat Resistance to T. gondii growth and is the precursor for the synthesis of L-glutamine, Lproline and polyamines via the ornithine decarboxylase pathway. Polyamines are essential for the proliferation of cells and parasites. Furthermore, the potential pathological effects of high NO throughput are limited because arginase competes with 10455325 iNOS for the same substrate, and it has been established that arginase activity modulates NO production by reducing the availability of L-arginine to iNOS. It has long been known that rat macrophages are naturally resistant to T. gondii infection. However, the mechanism of this resistance has not been reported. Many studies have demonstrated that NO can inhibit T. gondii proliferation in mouse macrophages after being stimulated with LPS or other cytokines. It has also been shown that in rat and mouse, NOS and arginase activity levels are different in resident peritoneal macrophages. Herein, we raise the questions of whether NO in rat macrophages plays a key role in their resistance to T. gondii BAY-41-2272 infection and whether there is any interaction between arginase and iNOS in the rat macrophage that could explain the rat’s resistance to T gondii infection. The aim of this study is to investigate whether host iNOS and arginase are opposing markers of resistance/susceptibility to T. gondii infection in rodent macrophages contrast, a significantly lower number of T. gondii were found in rat peritoneal macrophages. These results confirm previous studies and demonstrate the comparability of our system. Through fluorescent microscopy and Wright-Giemsa staining of infected cells, we found that after 24 hrs of T. gondii infection there were, on average, only one or two parasites in rat macrophages compared to more than 14 parasites in mouse cells, indicating that rat macrophages exhibit high resistance to T. gondii. Interestingly, a greater number of parasites were found in the peritoneal macrophages from the BN rat in which we detected a lower level of NO. The BN rat has been reported to be more sensitive to other strains of T. gondii, such as the Prugniaud strain. Accordingly, we hypothesized that NO could be an important factor involved in rat peritoneal macrophage resistance