The thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.

<h4>Background</h4>G. hollisae thermostable direct hemolysin (Gh-TDH) is produced by most strains of G. hollisae. This toxin has been reported to be absorbed in the intestines in humans. Secondary liver injury might be caused by venous return of the toxin through the portal system. We ai...

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Autores principales: Yan-Ren Lin, Yao-Li Chen, Keh-Bin Wang, Yi-Fang Wu, Yu-Kuo Wang, Sheng-Cih Huang, Tzu-An Liu, Manoswini Nayak, Bak-Sau Yip, Tung-Kung Wu
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spelling oai:doaj.org-article:dc98efab097b452d86abc0ce12bfb2e32021-11-18T07:56:37ZThe thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.1932-620310.1371/journal.pone.0056226https://doaj.org/article/dc98efab097b452d86abc0ce12bfb2e32013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23437095/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>G. hollisae thermostable direct hemolysin (Gh-TDH) is produced by most strains of G. hollisae. This toxin has been reported to be absorbed in the intestines in humans. Secondary liver injury might be caused by venous return of the toxin through the portal system. We aimed to firstly analyze the in vitro and in vivo hepatotoxicity of Gh-TDH.<h4>Methods</h4>Liver cells (primary human non-cancer cell and FL83B mouse cells) were treated and mice (BALB/c) were fed with this toxin to investigate its hepatotoxicity. Morphological examination and cytotoxicity assays using liver cells were also performed. Fluorescein isothiocyanate-conjugated toxin was used to analyze the localization of this protein in liver cells. Mice were subjected to liver function measurements and liver biopsies following toxin treatment and wild-type bacterial infection. PET (positron emission tomography)/CT (computed tomography) images were taken to assess liver metabolism during acute injury and recovery.<h4>Results</h4>The effect of hepatotoxicity was dose and time dependent. Cellular localization showed that the toxin was initially located around the cellular margins and subsequently entered the nucleus. Liver function measurements and liver biopsies of the mice following treatment with toxin or infection with wild-type Grimontia hollisae showed elevated levels of transaminases and damage to the periportal area, respectively. The PET/CT images revealed that the reconstruction of the liver continued for at least one week after exposure to a single dose of the toxin or bacterial infection.<h4>Conclusions</h4>The hepatotoxicity of Gh-TDH was firstly demonstrated. The damage was located in the periportal area of the liver, and the liver became functionally insufficient.Yan-Ren LinYao-Li ChenKeh-Bin WangYi-Fang WuYu-Kuo WangSheng-Cih HuangTzu-An LiuManoswini NayakBak-Sau YipTung-Kung WuPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 2, p e56226 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Yan-Ren Lin
Yao-Li Chen
Keh-Bin Wang
Yi-Fang Wu
Yu-Kuo Wang
Sheng-Cih Huang
Tzu-An Liu
Manoswini Nayak
Bak-Sau Yip
Tung-Kung Wu
The thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.
description <h4>Background</h4>G. hollisae thermostable direct hemolysin (Gh-TDH) is produced by most strains of G. hollisae. This toxin has been reported to be absorbed in the intestines in humans. Secondary liver injury might be caused by venous return of the toxin through the portal system. We aimed to firstly analyze the in vitro and in vivo hepatotoxicity of Gh-TDH.<h4>Methods</h4>Liver cells (primary human non-cancer cell and FL83B mouse cells) were treated and mice (BALB/c) were fed with this toxin to investigate its hepatotoxicity. Morphological examination and cytotoxicity assays using liver cells were also performed. Fluorescein isothiocyanate-conjugated toxin was used to analyze the localization of this protein in liver cells. Mice were subjected to liver function measurements and liver biopsies following toxin treatment and wild-type bacterial infection. PET (positron emission tomography)/CT (computed tomography) images were taken to assess liver metabolism during acute injury and recovery.<h4>Results</h4>The effect of hepatotoxicity was dose and time dependent. Cellular localization showed that the toxin was initially located around the cellular margins and subsequently entered the nucleus. Liver function measurements and liver biopsies of the mice following treatment with toxin or infection with wild-type Grimontia hollisae showed elevated levels of transaminases and damage to the periportal area, respectively. The PET/CT images revealed that the reconstruction of the liver continued for at least one week after exposure to a single dose of the toxin or bacterial infection.<h4>Conclusions</h4>The hepatotoxicity of Gh-TDH was firstly demonstrated. The damage was located in the periportal area of the liver, and the liver became functionally insufficient.
format article
author Yan-Ren Lin
Yao-Li Chen
Keh-Bin Wang
Yi-Fang Wu
Yu-Kuo Wang
Sheng-Cih Huang
Tzu-An Liu
Manoswini Nayak
Bak-Sau Yip
Tung-Kung Wu
author_facet Yan-Ren Lin
Yao-Li Chen
Keh-Bin Wang
Yi-Fang Wu
Yu-Kuo Wang
Sheng-Cih Huang
Tzu-An Liu
Manoswini Nayak
Bak-Sau Yip
Tung-Kung Wu
author_sort Yan-Ren Lin
title The thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.
title_short The thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.
title_full The thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.
title_fullStr The thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.
title_full_unstemmed The thermostable direct hemolysin from Grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.
title_sort thermostable direct hemolysin from grimontia hollisae causes acute hepatotoxicity in vitro and in vivo.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/dc98efab097b452d86abc0ce12bfb2e3
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