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Toxoplasma gondii infection can regulate the expression of tumour necorsis factor-α receptors on human cell in vitro.

Authors :
Derouich-Guergour, Dorra
Aldebert, Delphine
Vigan, Ines
Jouvin-Marche, Evelyne
Marche, Patrice N.
Aubert, Dominique
Ambroise-Thomas, Pierre
Pelloux, Hervé
Source :
Parasite Immunology; May2002, Vol. 24 Issue 5, p271-279, 9p
Publication Year :
2002

Abstract

Summary The in vitro regulation of tumour necrosis factor (TNF)-α receptors during Toxoplasma gondii infection of human MRC5 fibroblasts and human myelomonocytic THP-1 cells was investigated. Cells were infected with the virulent RH of T. gondii. TNFR membrane receptors were analysed by flow cytometry with biotinylated TNF-α. Shedding of the soluble form of TNFR1 and TNFR2 in cell culture supernatants was measured by enzyme-linked immunosorbent assay, and expression of mRNA production of TNFR1 and TNFR2 was analysed by quantitative real-time ploymerase chain reaction, 1 h after infection. In the MRC5 cell line, T. gondii infection did not induce any up- or down-regulation of membrane TNFRs, soluble TNFRs or mRNA of TNFRs. However, THP-1 cell infection with living parasites induced a significant soluble TNFR1 release by THP-1 cells after 1 h. We detected an approximately 50% up-regulation (P < 0·01) of soluble TNFR1 in infected THP-1 cells compared to controls. No change in soluble TNFR2 levels was observed in the same conditions. Moreover, infection decreased the level of TNF membrane receptors, but had no effect on TNFR1 and TNFR2 mRNA levels. TNFR modulation by T. gondii infection, in vitro, depends on the cell type. Furthermore, our data suggest that living parasites control the shedding of the soluble form of TNFR1. This mechanism may influence the role of TNF-α in toxoplasmosis. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
01419838
Volume :
24
Issue :
5
Database :
Complementary Index
Journal :
Parasite Immunology
Publication Type :
Academic Journal
Accession number :
6772800
Full Text :
https://doi.org/10.1046/j.1365-3024.2002.00462.x