IL-4 Independent Nuclear Translocalization of STAT6 in HeLa Cells by Entry of Toxoplasma gondii.
10.3347/kjp.2009.47.2.117
- Author:
Hye Jin AHN
1
;
Ji Yeon KIM
;
Ho Woo NAM
Author Information
1. Department of Parasitology and Catholic Institute of Parasitic Diseases, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea. howoo@catholic.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Toxoplasma gondii;
entry;
STAT6 phosphorylation;
nuclear translocation;
STAT1;
IL-4;
IFN-gamma
- MeSH:
Active Transport, Cell Nucleus;
Animals;
Chemokines, CC/biosynthesis;
Hela Cells;
Humans;
Interleukin-4/*immunology;
Mice;
Mice, Inbred BALB C;
STAT6 Transcription Factor/*immunology/*metabolism;
Toxoplasma/*immunology
- From:The Korean Journal of Parasitology
2009;47(2):117-124
- CountryRepublic of Korea
- Language:English
-
Abstract:
Toxoplasma gondii provokes rapid and sustained nuclear translocation of the signal transducer and activator of transcription 6 (STAT6) in HeLa cells. We observed activation of STAT6 as early as 2 hr after infection with T. gondii by the nuclear translocation of fluorescence expressed from exogenously transfected pDsRed2-STAT6 plasmid and by the detection of phosphotyrosine-STAT6 in Western blot. STAT6 activation occurred only by infection with live tachyzoites but not by co-culture with killed tachyzoites or soluble T. gondii extracts. STAT6 phosphorylation was inhibited by small interfering RNA of STAT6 (siSTAT6). In view of the fact that STAT6 is a central mediator of IL-4 induced gene expression, activation of STAT6 by T. gondii infection resembles that infected host cells has been stimulated by IL-4 treatment. STAT1 was affected to increase the transcription and expression by the treatment of siSTAT6. STAT6 activation was not affected by any excess SOCS's whereas that with IL-4 was inhibited by SOCS-1 and SOCS-3. T. gondii infection induced Eotaxin-3 gene expression which was reduced by IFN-gamma. These results demonstrate that T. gondii exploits host STAT6 to take away various harmful reactions by IFN-gamma. This shows, for the first time, IL-4-like action by T. gondii infection modulates microbicidal action by IFN-gamma in infected cells.
