| Autor: |
Zhao ZJ; State Key Laboratory of Biocontrol, Center for Parasitic Organisms, School of Life Sciences, Sun Yat-Sen University, Guangzhou, PR China., Zhang J, Wei J, Li Z, Wang T, Yi SQ, Shen JL, Yang TB, Hide G, Lun ZR |
| Jazyk: |
angličtina |
| Zdroj: |
PloS one [PLoS One] 2013 May 15; Vol. 8 (5), pp. e63650. Date of Electronic Publication: 2013 May 15 (Print Publication: 2013). |
| DOI: |
10.1371/journal.pone.0063650 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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