دورية أكاديمية
أعرض في EDS

Drug-induced allergic hepatitis develops in mice when myeloid-derived suppressor cells are depleted prior to halothane treatment.

التفاصيل البيبلوغرافية
العنوان: Drug-induced allergic hepatitis develops in mice when myeloid-derived suppressor cells are depleted prior to halothane treatment.
المؤلفون: Chakraborty M; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Fullerton AM; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Semple K; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Chea LS; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Proctor WR; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Bourdi M; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Kleiner DE; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD., Zeng X; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Ryan PM; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Dagur PK; Hematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Berkson JD; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD., Reilly TP; Exploratory Clinical & Translational Research, Bristol-Myers Squibb Company, Princeton, NJ., Pohl LR; Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD.
المصدر: Hepatology (Baltimore, Md.) [Hepatology] 2015 Aug; Vol. 62 (2), pp. 546-57. Date of Electronic Publication: 2015 Mar 25.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Wolters Kluwer Health, Inc Country of Publication: United States NLM ID: 8302946 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1527-3350 (Electronic) Linking ISSN: 02709139 NLM ISO Abbreviation: Hepatology Subsets: MEDLINE
أسماء مطبوعة: Publication: 2023- : [Philadelphia] : Wolters Kluwer Health, Inc.
Original Publication: Baltimore, MD : Williams & Wilkins, [c1981]-
مواضيع طبية MeSH: CD11b Antigen/*immunology , CD8-Positive T-Lymphocytes/*immunology , Chemical and Drug Induced Liver Injury/*immunology , Halothane/*toxicity , Hepatitis/*immunology , Myeloid Cells/*metabolism, Alanine Transaminase/metabolism ; Analysis of Variance ; Animals ; CD11b Antigen/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Cell Proliferation ; Chemical and Drug Induced Liver Injury/pathology ; Disease Models, Animal ; Female ; Flow Cytometry ; Hepatitis/pathology ; Immunohistochemistry ; Mice ; Mice, Inbred BALB C ; Myeloid Cells/drug effects ; Nitric Oxide/metabolism ; Random Allocation
مستخلص: Unlabelled: Clinical evidence suggests that many cases of serious idiosyncratic drug-induced liver injury are mediated by the adaptive immune system in response to hepatic drug-protein adducts, also referred to as "drug-induced allergic hepatitis"; but detailed mechanistic proof has remained elusive due to the lack of animal models. We have hypothesized that drug-induced allergic hepatitis is as rare in animals as it is in humans due at least in part to the tolerogenic nature of the liver. We provide evidence that immune tolerance can be overcome in a murine model of halothane-induced liver injury initiated by trifluoroacetylated protein adducts of halothane formed in the liver. Twenty-four hours after female Balb/cJ mice were initially treated with halothane, perivenous necrosis and an infiltration of CD11b(+) Gr-1(high) cells were observed in the liver. Further study revealed a subpopulation of myeloid-derived suppressor cells within the CD11b(+) Gr-1(high) cell fraction that inhibited the proliferation of both CD4(+) and CD8(+) T cells. When CD11b(+) Gr-1(high) cells were depleted from the liver with Gr-1 antibody treatment, enhanced liver injury was observed at 9 days after halothane rechallenge. Toxicity was associated with increased serum levels of interleukin-4 and immunoglobulins G1 and E directed against hepatic trifluoroacetylated protein adducts, as well as increased hepatic infiltration of eosinophils and CD4(+) T cells, all features of an allergic reaction. When hepatic CD4(+) T cells were depleted 5 days after halothane rechallenge, trifluoroacetylated protein adduct-specific serum immunoglobulin and hepatotoxicity were reduced.
Conclusion: Our data provide a rational approach for developing animal models of drug-induced allergic hepatitis mediated by the adaptive immune system and suggest that impaired liver tolerance may predispose patients to this disease.
(© 2015 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.)
التعليقات: Comment in: Hepatology. 2015 Aug;62(2):346-8. (PMID: 25833746)
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معلومات مُعتمدة: Z99 HL999999 United States Intramural NIH HHS
المشرفين على المادة: 0 (CD11b Antigen)
31C4KY9ESH (Nitric Oxide)
EC 2.6.1.2 (Alanine Transaminase)
UQT9G45D1P (Halothane)
تواريخ الأحداث: Date Created: 20150226 Date Completed: 20151013 Latest Revision: 20200225
رمز التحديث: 20240829
مُعرف محوري في PubMed: PMC6528654
DOI: 10.1002/hep.27764
PMID: 25712247
قاعدة البيانات: MEDLINE
الوصف
تدمد:1527-3350
DOI:10.1002/hep.27764