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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
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 numb...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3655142/ https://www.ncbi.nlm.nih.gov/pubmed/23691079 http://dx.doi.org/10.1371/journal.pone.0063650 |
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author | Zhao, Zhi-Jun Zhang, Jia Wei, Jun Li, Zhi Wang, Tao Yi, Si-Qi Shen, Ji-Long Yang, Ting-Bao Hide, Geoff Lun, Zhao-Rong |
author_facet | Zhao, Zhi-Jun Zhang, Jia Wei, Jun Li, Zhi Wang, Tao Yi, Si-Qi Shen, Ji-Long Yang, Ting-Bao Hide, Geoff Lun, Zhao-Rong |
author_sort | Zhao, Zhi-Jun |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3655142 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-36551422013-05-20 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 Zhao, Zhi-Jun Zhang, Jia Wei, Jun Li, Zhi Wang, Tao Yi, Si-Qi Shen, Ji-Long Yang, Ting-Bao Hide, Geoff Lun, Zhao-Rong PLoS One Research Article 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. Public Library of Science 2013-05-15 /pmc/articles/PMC3655142/ /pubmed/23691079 http://dx.doi.org/10.1371/journal.pone.0063650 Text en © 2013 Zhao et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Zhao, Zhi-Jun Zhang, Jia Wei, Jun Li, Zhi Wang, Tao Yi, Si-Qi Shen, Ji-Long Yang, Ting-Bao Hide, Geoff Lun, Zhao-Rong 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 |
title | 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 |
title_full | 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 |
title_fullStr | 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 |
title_full_unstemmed | 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 |
title_short | 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 |
title_sort | 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 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3655142/ https://www.ncbi.nlm.nih.gov/pubmed/23691079 http://dx.doi.org/10.1371/journal.pone.0063650 |
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