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The gene expression level of IFN-?R1 and IFN-?R2 in a murine model treated with Toxoplasma gondii and its products.

ABSTRACT: AIM:To evaluate the effect of active T. gondii tachyzoites and its products on the gene expression level of IFN-?R1 and IFN-?R2 in a murine model. BACKGROUND:Many studies have shown that the parasite Toxoplasma gondii utilizes different mechanisms to inhibit the function of IFN-?, but the parasite effect on the function of IFN-?R1 and IFN-?R2 is still unclear. PATIENTS AND METHODS:Toxoplasma lysate product (TLP), excretory/secretory products (ESPs) obtained from cell free and cell culture media as well as active tachyzoites were injected separately to their respective group each consisted of 10 BALB/c mice. One control group of 10 mice received phosphate buffered saline (PBS). All of the mice were euthanized three days after the last injection and then their peritoneal leukocytes were harvested separately. The total RNA was extracted from the samples, converted to cDNA, and the gene expression level of IFN-?R1 and IFN-?R2 was assessed in all of the treated groups relative to the control one. RESULTS:There was no significant difference between each of the treated groups relative to the control group concerning the gene expression level of IFN-?R2 (P> 0.05). Furthermore, the gene expression level of IFN-?R1 in two groups of TLP (P= 0.04) and ESP obtained from cell free medium (P= 0.008) showed a significant difference relative to the control group. CONCLUSION:Findings of this study revealed a new aspect of host-T. gondii interaction in that this parasite is able to downregulate IFN-?R1 to reduce the IFN-? effects on the infected cell.

SUBMITTER: Kalani H

PROVIDER: S-EPMC4833851 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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The gene expression level of IFN-γR1 and IFN-γR2 in a murine model treated with Toxoplasma gondii and its products.

Kalani Hamed H Khanahmad Shahreza Hosein H Daryani Ahmad A Yousefi Hosein Ali HA Pestechian Nader N Mansouri Vahid V

Gastroenterology and hepatology from bed to bench 20160101 2

<h4>Aim</h4>To evaluate the effect of active T. gondii tachyzoites and its products on the gene expression level of IFN-γR1 and IFN-γR2 in a murine model.<h4>Background</h4>Many studies have shown that the parasite Toxoplasma gondii utilizes different mechanisms to inhibit the function of IFN-γ, but the parasite effect on the function of IFN-γR1 and IFN-γR2 is still unclear.<h4>Patients and methods</h4>Toxoplasma lysate product (TLP), excretory/secretory products (ESPs) obtained from cell free a ...[more]

PMID: 27099672

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Project description:Toxoplasma gondii is the most common protozoan parasitic infection in man. Gamma interferon (IFN?) activates haematopoietic and non-haematopoietic cells to kill the parasite and mediate host resistance. IFN?-driven host resistance pathways and parasitic virulence factors are well described in mice, but a detailed understanding of pathways that kill Toxoplasma in human cells is lacking. Here we show, that contrary to the widely held belief that the Toxoplasma vacuole is non-fusogenic, in an immune-stimulated environment, the vacuole of type II Toxoplasma in human cells is able to fuse with the host endo-lysosomal machinery leading to parasite death by acidification. Similar to murine cells, we find that type II, but not type I Toxoplasma vacuoles are targeted by K63-linked ubiquitin in an IFN?-dependent manner in non-haematopoetic primary-like human endothelial cells. Host defence proteins p62 and NDP52 are subsequently recruited to the type II vacuole in distinct, overlapping microdomains with a loss of IFN?-dependent restriction in p62 knocked down cells. Autophagy proteins Atg16L1, GABARAP and LC3B are recruited to <10% of parasite vacuoles and show no parasite strain preference, which is consistent with inhibition and enhancement of autophagy showing no effect on parasite replication. We demonstrate that this differs from HeLa human epithelial cells, where type II Toxoplasma are restricted by non-canonical autophagy leading to growth stunting that is independent of lysosomal acidification. In contrast to mouse cells, human vacuoles do not break. In HUVEC, the ubiquitinated vacuoles are targeted for destruction in acidified LAMP1-positive endo-lysosomal compartments. Consequently, parasite death can be prevented by inhibiting host ubiquitination and endosomal acidification. Thus, K63-linked ubiquitin recognition leading to vacuolar endo-lysosomal fusion and acidification is an important, novel virulence-driven Toxoplasma human host defence pathway.

Dataset Information

The gene expression level of IFN-?R1 and IFN-?R2 in a murine model treated with Toxoplasma gondii and its products.

Publications

The gene expression level of IFN-γR1 and IFN-γR2 in a murine model treated with Toxoplasma gondii and its products.

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