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Differences in iNOS and arginase expression and activity in the macrophages of rats are responsible for the resistance against T. gondii infection

Gruner, AC; Li, Z; Zhao, ZJ; Zhu, XQ; Ren, QS; Nie, FF; Gao, JM; Gao, XJ; Yang, TB; Zhou, WL; Shen, JL; Wang, Y; Lu, FL; Chen, XG; Hide, G; Ayala, FJ; Lun, ZR

Differences in iNOS and arginase expression and activity in the macrophages of rats are responsible for the resistance against T. gondii infection Thumbnail


Authors

AC Gruner

Z Li

ZJ Zhao

XQ Zhu

QS Ren

FF Nie

JM Gao

XJ Gao

TB Yang

WL Zhou

JL Shen

Y Wang

FL Lu

XG Chen

FJ Ayala

ZR Lun



Abstract

Toxoplasma gondii infects humans and warm blooded animals causing devastating disease worldwide. It has long been a
mystery as to why the peritoneal macrophages of rats are naturally resistant to T. gondii infection while those of mice are
not. Here, we report that high expression levels and activity of inducible nitric oxide synthase (iNOS) and low levels of
arginase-1 (Arg 1) activity in the peritoneal macrophages of rats are responsible for their resistance against T. gondii
infection, due to high nitric oxide and low polyamines within these cells. The opposite situation was observed in the
peritoneal macrophages of mice. This discovery of the opposing functions of iNOS and Arg 1 in rodent peritoneal
macrophages may lead to a better understanding of the resistance mechanisms of mammals, particularly humans and
livestock, against T. gondii and other intracellular pathogens.

Citation

Gruner, A., Li, Z., Zhao, Z., Zhu, X., Ren, Q., Nie, F., …Lun, Z. (2012). Differences in iNOS and arginase expression and activity in the macrophages of rats are responsible for the resistance against T. gondii infection. PLoS ONE, 7(4), e35834. https://doi.org/10.1371/journal.pone.0035834

Journal Article Type Article
Publication Date Jan 1, 2012
Deposit Date Sep 11, 2012
Publicly Available Date Apr 5, 2016
Journal PLoS ONE
Publisher Public Library of Science
Peer Reviewed Peer Reviewed
Volume 7
Issue 4
Pages e35834
DOI https://doi.org/10.1371/journal.pone.0035834
Publisher URL http://dx.doi.org/10.1371/journal.pone.0035834

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