val of hosts during T. gondii and Mycobacterium tuberculosis infections, because more arginine is available to produce NO. In conclusion, our results demonstrate that the different Chrysontemin site expression levels of iNOS and Arg 1 in rodent peritoneal macrophages work together to determine the resistance and susceptibility to T. gondii RH strain infection. High iNOS and low Arg 1 expression level in the rat peritoneal macrophages result in the natural resistance to T. gondii infection. In contrast, low iNOS and high Arg 21278085” 1 expression level in mouse peritoneal macrophages allow the growth of T. gondii. The present study highlights the NOdependent immunity to T. gondii and the opposing roles of iNOS and Arg 1 to the growth of the parasite in rat macrophages. These findings provide insights towards understanding the mechanisms used by mammals against infections of T. gondii and other intracellular pathogens. Furthermore, the differences in iNOS and Arg 1 activity between individual inbred lines of mice and rats indicates that this mechanism may also account for variation in susceptibility of individuals within natural populations of mammalian species. Further study of these processes may lead to a better understanding of the mechanisms of parasite virulence and host resistance. Such an understanding is likely to improve our ability to develop drugs against T. gondii. Materials and Methods Ethics Statement All animals were treated in strict accordance to the guidelines for the Laboratory Animal Use and Care from Chinese CDC and the Rules for Medical Laboratory 17622149” Animals from Ministry of Health, China, under the protocols approved by National Institute for Communicable Disease Control and Prevention and Laboratory Animal Use and Care Committee of Sun Yat-Sen University under the licenses of 2010CB53000. Animals We used five rat strains, Sprague Dawley, Wistar, Brown Norway, Fischer 344 and Lewis and 4 mouse strains, BALB/c, C57BL/6, NIH and Swiss mice. All BN, F344 and Lewis were purchased from Vital River Laboratories; the other rat and mouse strains were purchased from the Experimental Animal Center of Sun Yat-Sen University. All animals were maintained in a pathogen-free room at the School of Life Sciences, Sun Yat-Sen University following the university policy. 7 Mechanism of Rat Resistance to T. gondii BN6 Lewis F1 progeny BN 6 Lewis F1 hybrid rats were generated in our laboratory, which were viably fertile, normal in size and did not display any behavioral or physical abnormalities. F1 individuals were identified by a black and white pattern on the underside. USA) with 10% fetal bovine serum for further use after counted. Peritoneal macrophage isolation and cultivation Animals, sacrificed by carbon dioxide, were injected intraperitoneally with 5 ml or 15 ml ice cold DHank’s solution containing 100 U of penicillin and 100 mg of streptomycin per ml and then peritoneal cells were harvested and separated by centrifugation at 2506g for 10 min at 4uC. The cells were washed by D-Hank’s solution and centrifuged with the same procedure. Finally, cells were suspended in RPMI-1640 medium with 10% FBS and 
left to adhere for 2 hrs at 37uC in an incubator containing 5% CO2 and 95% air. Non-adherent cells were removed and fresh medium was added. Macrophages were cultured overnight and then used for further experiments. Rat peritoneal macrophages were incubated with or without lipopolysaccharide plus IFN-c or with the NOS specific inhibitor Nv Parasites The Toxoplasma
