Involvement of MAPK activation in chemokine or COX-2 productions by Toxoplasma gondii.
10.3347/kjp.2006.44.3.197
- Author:
Ji Young KIM
1
;
Myoung Hee AHN
;
Hyun Ouk SONG
;
Jong Hak CHOI
;
Jae Sook RYU
;
Duk Young MIN
;
Myung Hwan CHO
Author Information
1. Department of Parasitology, Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, 133-791, Korea. mhahn@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
Toxoplasma gondii;
mitogen activated protein kinase (MAPK);
chemokine;
cyclooxygenase-2;
prostaglandin E2
- MeSH:
Toxoplasmosis/*enzymology/*immunology;
Toxoplasma/*immunology/*metabolism;
Mitogen-Activated Protein Kinases/*metabolism;
Mice, Inbred BALB C;
Mice;
Macrophages, Peritoneal/enzymology/immunology/parasitology;
Humans;
Hela Cells;
Enzyme Activation;
Cyclooxygenase 2/*biosynthesis;
Chemokines/*biosynthesis;
Animals
- From:The Korean Journal of Parasitology
2006;44(3):197-207
- CountryRepublic of Korea
- Language:English
-
Abstract:
This experiment focused on MAPK activation in host cell invasion and replication of T. gondii, as well as the expression of CC chemokines, MCP-1 and MIP-1 alpha , and enzyme, COX-2/prostaglandin E2 (PGE2) in infected cells via western blot, [3H]-uracil incorporation assay, ELISA and RT-PCR. The phosphorylation of ERK1/2 and p38 in infected HeLa cells was detected at 1 hr and/or 6 hr postinfection (PI). Tachyzoite proliferation was reduced by p38 or JNK MAPK inhibitors. MCP-1 secretion was enhanced in infected peritoneal macrophages at 6 hr PI. MIP-1 alpha mRNA was increased in macrophages at 18 hr PI. MCP-1 and MIP-1 alpha were reduced after treatment with inhibitors of ERK1/2 and JNK MAPKs. COX-2 mRNA gradually increased in infected RAW 264.7 cells and the secretion of COX-2 peaked at 6 hr PI. The inhibitor of JNK suppressed COX-2 expression. PGE2 from infected RAW 264.7 cells was increased and synthesis was suppressed by PD98059, SB203580, and SP600125. In this study, the activation of p38, JNK and/or ERK1/2 MAPKs occurred during the invasion and proliferation of T. gondii tachyzoites in HeLa cells. Also, increased secretion and expression of MCP-1, MIP-1 alpha , COX-2 and PGE2 were detected in infected macrophages, and appeared to occur via MAPK signaling pathways.
