학술논문

The gene expression level of IFN-γR1 and IFN-γR2 in a murine model treated with Toxoplasma gondii and its products.
Document Type
Article
Source
Gastroenterology & Hepatology from Bed to Bench. Spring2016, Vol. 9 Issue 2, p124-131. 8p. 3 Charts, 1 Graph.
Subject
*INFECTION
*RNA physiology
*ANIMAL experimentation
*GASTROENTEROLOGY
*GENE expression
*HOSPITAL gastroenterology services
*INTERFERONS
*MICE
*PARASITES
*PARASITIC diseases
*POLYMERASE chain reaction
*PROTOZOA
*RESEARCH funding
*TOXOPLASMOSIS
*DATA analysis
*DESCRIPTIVE statistics
*DIAGNOSIS
Language
ISSN
2008-2258
Abstract
Aim: 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. Background: 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. 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-γR1 and IFN-γR2 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-γR2 (P> 0.05). Furthermore, the gene expression level of IFN-γR1 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-γR1 to reduce the IFN-γ effects on the infected cell. [ABSTRACT FROM AUTHOR]