Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells

DT388GMCSF, a fusion toxin composed of the NH2-terminal region of diphtheria toxin (DT) fused to human granulocyte-macrophage colony-stimulating factor (GMCSF) has shown efficacy in the treatment of acute myeloid leukemia. However, the primary dose-limiting side effect is liver toxicity. We have rep...

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محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Abi-Habib, Ralph J. (author)
مؤلفون آخرون: Westcott, Marlena (author), Cohen, Kimberley (author), Willingham, Mark (author), Lui, Shihui (author), Bugge, Thomas (author), Leppla, Stephen H. (author), Frankel, Arthur (author)
التنسيق: article
منشور في: 2004
الوصول للمادة أونلاين:http://hdl.handle.net/10725/2736
http://mct.aacrjournals.org/content/3/12/1681.short
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_version_ 1864513459125747712
author Abi-Habib, Ralph J.
author2 Westcott, Marlena
Cohen, Kimberley
Willingham, Mark
Lui, Shihui
Bugge, Thomas
Leppla, Stephen H.
Frankel, Arthur
author2_role author
author
author
author
author
author
author
author_facet Abi-Habib, Ralph J.
Westcott, Marlena
Cohen, Kimberley
Willingham, Mark
Lui, Shihui
Bugge, Thomas
Leppla, Stephen H.
Frankel, Arthur
author_role author
dc.creator.none.fl_str_mv Abi-Habib, Ralph J.
Westcott, Marlena
Cohen, Kimberley
Willingham, Mark
Lui, Shihui
Bugge, Thomas
Leppla, Stephen H.
Frankel, Arthur
dc.date.none.fl_str_mv 2004
2015-11-30T11:50:11Z
2015-11-30T11:50:11Z
2016-05-10
dc.identifier.none.fl_str_mv 1535-7163
http://hdl.handle.net/10725/2736
Westcott, M. M., Abi-Habib, R. J., Cohen, K. A., Willingham, M. C., Liu, S., Bugge, T. H., ... & Frankel, A. E. (2004). Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells. Molecular cancer therapeutics, 3(12), 1681-1689.
http://mct.aacrjournals.org/content/3/12/1681.short
dc.language.none.fl_str_mv en
dc.relation.none.fl_str_mv Molecular cancer therapeutics
dc.rights.*.fl_str_mv info:eu-repo/semantics/openAccess
dc.title.none.fl_str_mv Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
dc.type.none.fl_str_mv Article
info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/article
description DT388GMCSF, a fusion toxin composed of the NH2-terminal region of diphtheria toxin (DT) fused to human granulocyte-macrophage colony-stimulating factor (GMCSF) has shown efficacy in the treatment of acute myeloid leukemia. However, the primary dose-limiting side effect is liver toxicity. We have reproduced liver toxicity in rats using the rodent cell-tropic DT-murine GMCSF (DT390mGMCSF). Serum aspartate aminotransferase and alanine aminotransferase were elevated 15- and 4-fold, respectively, in DT390mGMCSF-treated rats relative to controls. Histologic analysis revealed hepatocyte swelling; however, this did not lead to hepatic necrosis or overt histopathologic changes in the liver. Immunohistochemical staining showed apoptotic cells in the sinusoids, and depletion of cells expressing the monocyte/macrophage markers, ED1 and ED2, indicating that Kupffer cells (KC) are targets of DT390mGMCSF. In contrast, sinusoidal endothelial cells seemed intact. In vitro, DT390mGMCSF was directly cytotoxic to primary KC but not hepatocytes. Two related fusion toxins, DT388GMCSF, which targets the human GMCSF receptor, and DT390mIL-3, which targets the rodent IL-3 receptor, induced a less than 2-fold elevation in serum transaminases and did not deplete KC in vivo. In addition, DTU2mGMCSF, a modified form of DT390mGMCSF with enhanced tumor cell specificity, was not hepatotoxic and was significantly less toxic to KC in vivo and in vitro. These results show that DT390mGMCSF causes liver toxicity by targeting KC, and establish a model for studying how this leads to hepatocyte injury. Furthermore, alternative fusion toxins with potentially reduced hepatotoxicity are presented.
eu_rights_str_mv openAccess
format article
id LAURepo_41bd7d4cba6f9a0bcb57363467939f2e
identifier_str_mv 1535-7163
Westcott, M. M., Abi-Habib, R. J., Cohen, K. A., Willingham, M. C., Liu, S., Bugge, T. H., ... & Frankel, A. E. (2004). Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells. Molecular cancer therapeutics, 3(12), 1681-1689.
language_invalid_str_mv en
network_acronym_str LAURepo
network_name_str Lebanese American University repository
oai_identifier_str oai:laur.lau.edu.lb:10725/2736
publishDate 2004
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repository.name.fl_str_mv
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spelling Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cellsAbi-Habib, Ralph J.Westcott, MarlenaCohen, KimberleyWillingham, MarkLui, ShihuiBugge, ThomasLeppla, Stephen H.Frankel, ArthurDT388GMCSF, a fusion toxin composed of the NH2-terminal region of diphtheria toxin (DT) fused to human granulocyte-macrophage colony-stimulating factor (GMCSF) has shown efficacy in the treatment of acute myeloid leukemia. However, the primary dose-limiting side effect is liver toxicity. We have reproduced liver toxicity in rats using the rodent cell-tropic DT-murine GMCSF (DT390mGMCSF). Serum aspartate aminotransferase and alanine aminotransferase were elevated 15- and 4-fold, respectively, in DT390mGMCSF-treated rats relative to controls. Histologic analysis revealed hepatocyte swelling; however, this did not lead to hepatic necrosis or overt histopathologic changes in the liver. Immunohistochemical staining showed apoptotic cells in the sinusoids, and depletion of cells expressing the monocyte/macrophage markers, ED1 and ED2, indicating that Kupffer cells (KC) are targets of DT390mGMCSF. In contrast, sinusoidal endothelial cells seemed intact. In vitro, DT390mGMCSF was directly cytotoxic to primary KC but not hepatocytes. Two related fusion toxins, DT388GMCSF, which targets the human GMCSF receptor, and DT390mIL-3, which targets the rodent IL-3 receptor, induced a less than 2-fold elevation in serum transaminases and did not deplete KC in vivo. In addition, DTU2mGMCSF, a modified form of DT390mGMCSF with enhanced tumor cell specificity, was not hepatotoxic and was significantly less toxic to KC in vivo and in vitro. These results show that DT390mGMCSF causes liver toxicity by targeting KC, and establish a model for studying how this leads to hepatocyte injury. Furthermore, alternative fusion toxins with potentially reduced hepatotoxicity are presented.PublishedN/A2015-11-30T11:50:11Z2015-11-30T11:50:11Z20042016-05-10Articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1535-7163http://hdl.handle.net/10725/2736Westcott, M. M., Abi-Habib, R. J., Cohen, K. A., Willingham, M. C., Liu, S., Bugge, T. H., ... & Frankel, A. E. (2004). Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells. Molecular cancer therapeutics, 3(12), 1681-1689.http://mct.aacrjournals.org/content/3/12/1681.shortenMolecular cancer therapeuticsinfo:eu-repo/semantics/openAccessoai:laur.lau.edu.lb:10725/27362021-03-19T09:59:49Z
spellingShingle Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
Abi-Habib, Ralph J.
status_str publishedVersion
title Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
title_full Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
title_fullStr Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
title_full_unstemmed Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
title_short Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
title_sort Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor–induced hepatotoxicity is mediated by Kupffer cells
url http://hdl.handle.net/10725/2736
http://mct.aacrjournals.org/content/3/12/1681.short