Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica
The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and...
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The Korean Society for Parasitology and Tropical Medicine
2014
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Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4170031/ |
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pubmed-41700312014-09-22 Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica Lee, Young Ah Kim, Kyeong Ah Min, Arim Shin, Myeong Heon Original Article The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis. The Korean Society for Parasitology and Tropical Medicine 2014-08 2014-08-29 /pmc/articles/PMC4170031/ /pubmed/25246714 http://dx.doi.org/10.3347/kjp.2014.52.4.355 Text en © 2014, Korean Society for Parasitology and Tropical Medicine http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Lee, Young Ah Kim, Kyeong Ah Min, Arim Shin, Myeong Heon |
spellingShingle |
Lee, Young Ah Kim, Kyeong Ah Min, Arim Shin, Myeong Heon Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica |
author_facet |
Lee, Young Ah Kim, Kyeong Ah Min, Arim Shin, Myeong Heon |
author_sort |
Lee, Young Ah |
title |
Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica |
title_short |
Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica |
title_full |
Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica |
title_fullStr |
Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica |
title_full_unstemmed |
Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica |
title_sort |
amoebic pi3k and pkc is required for jurkat t cell death induced by entamoeba histolytica |
description |
The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis. |
publisher |
The Korean Society for Parasitology and Tropical Medicine |
publishDate |
2014 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4170031/ |
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1613135777749794816 |