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Rats are naturally resistant to  Toxoplasma gondii  infection, particularly the RH strain, while mice are not. Previous studies have demonstrated that inducible nitric oxide synthase (iNOS) and arginase-1 of rodent peritoneal macrophages are linked to the mechanism of resistance. As an increasing number of studies on human and animal infections are showing that pulmonary toxoplasmosis is one of the most severe clinical signs from  T. gondii  infection, we are interested to know whether  T. gondii  infection in alveolar macrophages of rats is also linked to the levels of iNOS and arginase-1 activity. Our results demonstrate that  T. gondii  could grow and proliferate in rat alveolar macrophages, both  in vitro  and  in vivo , at levels higher than resistant rat peritoneal macrophages and at comparable levels to sensitive mouse peritoneal macrophages. Lower activity and expression levels of iNOS and higher activity and expression levels of arginase-1 in rat alveolar macrophages were found to be linked to the susceptibility of  T. gondii  infection in these cells. These novel findings could aid a better understanding of the pathogenesis of clinical pulmonary toxoplasmosis in humans and domestic animals.

plos one

Lower Expression of Inducible Nitric Oxide Synthase and Higher Expression of Arginase in Rat Alveolar Macrophages Are Linked to Their Susceptibility to Toxoplasma gondii Infection