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Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro
The intestinal protozoan parasite, Giardia duodenalis, infects a large number of people in the world annually. Giardia infection has been considered a negative effect on intestinal epithelial cell growth, while the underlying mechanisms remain to be explored. Here we evaluated reactive oxygen specie...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7559850/ https://www.ncbi.nlm.nih.gov/pubmed/32842537 http://dx.doi.org/10.3390/pathogens9090693 |
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author | Liu, Lin Fang, Rui Wei, Ziyan Wu, Jingxue Li, Xiaoyun Li, Wei |
author_facet | Liu, Lin Fang, Rui Wei, Ziyan Wu, Jingxue Li, Xiaoyun Li, Wei |
author_sort | Liu, Lin |
collection | PubMed |
description | The intestinal protozoan parasite, Giardia duodenalis, infects a large number of people in the world annually. Giardia infection has been considered a negative effect on intestinal epithelial cell growth, while the underlying mechanisms remain to be explored. Here we evaluated reactive oxygen species (ROS) production and apoptotic events in Giardia trophozoites-stimulated Caco-2 cells via fluorescence microscopy, transmission electron microscopy, flow cytometry, western blot, and cell counting kit-8 analyses. The results showed that Giardia trophozoite treatment could induce lactate dehydrogenase release and Caco-2 cell apoptosis. The ROS levels were increased post treatment. The observed typical characteristics of mitochondria damage include significant swelling and degeneration of matrix and cristae. After trophozoite treatment, the level of Bax protein expression was increased, while Bcl-2 protein decreased. Trophozoite stimulation also led to reduction of mitochondrial membrane potential and release of cytochrome c from the mitochondria to the cytoplasm, and this process was accompanied by activation of caspase-9 and caspase-3 and poly (ADP-ribose) polymerase 1 cleavage. Pretreatment with N-acetyl-L-cysteine, a ROS inhibitor, reversed G. duodenalis-induced Caco-2 cell apoptosis. Taken together, we indicated that G. duodenalis could induce Caco-2 cell apoptosis through a ROS- and mitochondria-mediated caspase-dependent pathway. This study furthers our understanding of the cellular mechanism of the interaction between Giardia trophozoites and host cells. |
format | Online Article Text |
id | pubmed-7559850 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-75598502020-10-22 Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro Liu, Lin Fang, Rui Wei, Ziyan Wu, Jingxue Li, Xiaoyun Li, Wei Pathogens Article The intestinal protozoan parasite, Giardia duodenalis, infects a large number of people in the world annually. Giardia infection has been considered a negative effect on intestinal epithelial cell growth, while the underlying mechanisms remain to be explored. Here we evaluated reactive oxygen species (ROS) production and apoptotic events in Giardia trophozoites-stimulated Caco-2 cells via fluorescence microscopy, transmission electron microscopy, flow cytometry, western blot, and cell counting kit-8 analyses. The results showed that Giardia trophozoite treatment could induce lactate dehydrogenase release and Caco-2 cell apoptosis. The ROS levels were increased post treatment. The observed typical characteristics of mitochondria damage include significant swelling and degeneration of matrix and cristae. After trophozoite treatment, the level of Bax protein expression was increased, while Bcl-2 protein decreased. Trophozoite stimulation also led to reduction of mitochondrial membrane potential and release of cytochrome c from the mitochondria to the cytoplasm, and this process was accompanied by activation of caspase-9 and caspase-3 and poly (ADP-ribose) polymerase 1 cleavage. Pretreatment with N-acetyl-L-cysteine, a ROS inhibitor, reversed G. duodenalis-induced Caco-2 cell apoptosis. Taken together, we indicated that G. duodenalis could induce Caco-2 cell apoptosis through a ROS- and mitochondria-mediated caspase-dependent pathway. This study furthers our understanding of the cellular mechanism of the interaction between Giardia trophozoites and host cells. MDPI 2020-08-23 /pmc/articles/PMC7559850/ /pubmed/32842537 http://dx.doi.org/10.3390/pathogens9090693 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Liu, Lin Fang, Rui Wei, Ziyan Wu, Jingxue Li, Xiaoyun Li, Wei Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro |
title | Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro |
title_full | Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro |
title_fullStr | Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro |
title_full_unstemmed | Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro |
title_short | Giardia duodenalis Induces Apoptosis in Intestinal Epithelial Cells via Reactive Oxygen Species-Mediated Mitochondrial Pathway In Vitro |
title_sort | giardia duodenalis induces apoptosis in intestinal epithelial cells via reactive oxygen species-mediated mitochondrial pathway in vitro |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7559850/ https://www.ncbi.nlm.nih.gov/pubmed/32842537 http://dx.doi.org/10.3390/pathogens9090693 |
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