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ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells

Several animal models have shown that anthrax toxin (ATX) elicits a cytotoxic effect on host cells through anthrax toxin receptor (ANTXR) function. In this study, compared with mouse cells, cells obtained from humans exhibited low sensitivity to ATX-mediated cytotoxicity, and the sensitivity was not...

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Autores principales: FUJIKURA, Daisuke, TOYOMANE, Kochi, KAMIYA, Kozue, MUTOH, Memi, MIFUNE, Etsuko, OHNUMA, Miyuki, HIGASHI, Hideaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japanese Society of Veterinary Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053933/
https://www.ncbi.nlm.nih.gov/pubmed/27170489
http://dx.doi.org/10.1292/jvms.15-0727
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author FUJIKURA, Daisuke
TOYOMANE, Kochi
KAMIYA, Kozue
MUTOH, Memi
MIFUNE, Etsuko
OHNUMA, Miyuki
HIGASHI, Hideaki
author_facet FUJIKURA, Daisuke
TOYOMANE, Kochi
KAMIYA, Kozue
MUTOH, Memi
MIFUNE, Etsuko
OHNUMA, Miyuki
HIGASHI, Hideaki
author_sort FUJIKURA, Daisuke
collection PubMed
description Several animal models have shown that anthrax toxin (ATX) elicits a cytotoxic effect on host cells through anthrax toxin receptor (ANTXR) function. In this study, compared with mouse cells, cells obtained from humans exhibited low sensitivity to ATX-mediated cytotoxicity, and the sensitivity was not correlated with expression levels of ANTXRs. ATX treatment also induced a cytotoxic effect in other cultured human cells, human embryonic kidney (HEK) 293 cells, that express ANTXRs at undetectable levels. Furthermore, ectopic expression of ANTXRs in HEK293 cells did not affect the sensitivity to ATX treatment. These findings suggest that there is an ANTXR-independent cytotoxic mechanism in human cells.
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spelling pubmed-50539332016-10-07 ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells FUJIKURA, Daisuke TOYOMANE, Kochi KAMIYA, Kozue MUTOH, Memi MIFUNE, Etsuko OHNUMA, Miyuki HIGASHI, Hideaki J Vet Med Sci Bacteriology Several animal models have shown that anthrax toxin (ATX) elicits a cytotoxic effect on host cells through anthrax toxin receptor (ANTXR) function. In this study, compared with mouse cells, cells obtained from humans exhibited low sensitivity to ATX-mediated cytotoxicity, and the sensitivity was not correlated with expression levels of ANTXRs. ATX treatment also induced a cytotoxic effect in other cultured human cells, human embryonic kidney (HEK) 293 cells, that express ANTXRs at undetectable levels. Furthermore, ectopic expression of ANTXRs in HEK293 cells did not affect the sensitivity to ATX treatment. These findings suggest that there is an ANTXR-independent cytotoxic mechanism in human cells. The Japanese Society of Veterinary Science 2016-05-12 2016-08 /pmc/articles/PMC5053933/ /pubmed/27170489 http://dx.doi.org/10.1292/jvms.15-0727 Text en ©2016 The Japanese Society of Veterinary Science http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License.
spellingShingle Bacteriology
FUJIKURA, Daisuke
TOYOMANE, Kochi
KAMIYA, Kozue
MUTOH, Memi
MIFUNE, Etsuko
OHNUMA, Miyuki
HIGASHI, Hideaki
ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells
title ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells
title_full ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells
title_fullStr ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells
title_full_unstemmed ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells
title_short ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells
title_sort antxr-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells
topic Bacteriology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053933/
https://www.ncbi.nlm.nih.gov/pubmed/27170489
http://dx.doi.org/10.1292/jvms.15-0727
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