| Mifepristone (RU486) restores humoral and T cell-mediated immune response in endotoxin immunosuppressed mice. | |
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MedLine Citation:
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PMID: 20964639 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Sepsis and septic shock can be caused by Gram-positive and -negative bacteria and other microorganisms. In the case of Gram-negative bacteria, endotoxin, a normal constituent of the bacterial wall, also known as lipopolysaccharide (LPS), has been considered as one of the principal agents causing the undesirable effects in this critical illness. The response to LPS involves a rapid secretion of proinflammatory cytokines such as tumour necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, interferon (IFN)-γ and the concomitant induction of anti-inflammatory mediators such as IL-10, transforming growth factor (TGF)-β or glucocorticoids, which render the host temporarily refractory to subsequent lethal doses of LPS challenge in a process known as LPS or endotoxin tolerance. Although protective from the development of sepsis or systemic inflammation, endotoxin tolerance has also been pointed out as the main cause of the non-specific humoral and cellular immunosuppression described in these patients. In this report we demonstrate, using a mouse model, that mifepristone (RU486), a known glucocorticoid receptor antagonist, could play an important role in the restoration of both adaptive humoral and cellular immune response in LPS immunosuppressed mice, suggesting the involvement of endogenous glucocorticoids in this phenomenon. On the other hand, using cyclophosphamide and gemcitabine, we demonstrated that regulatory/suppressor CD4(+) CD25(+) forkhead boxP3(+) and GR-1(+) CD11b(+) cells do not play a major role in the establishment or the maintenance of endotoxin tolerance, a central mechanism for inducing an immunosuppression state. |
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Authors:
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B Rearte; A Maglioco; L Balboa; J Bruzzo; V I Landoni; E A Laborde; P Chiarella; R A Ruggiero; G C Fernández; M A Isturiz |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-10-21 |
Journal Detail:
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Title: Clinical and experimental immunology Volume: 162 ISSN: 1365-2249 ISO Abbreviation: Clin. Exp. Immunol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-12 Completed Date: 2011-03-08 Revised Date: 2011-12-21 |
Medline Journal Info:
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Nlm Unique ID: 0057202 Medline TA: Clin Exp Immunol Country: England |
Other Details:
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Languages: eng Pagination: 568-77 Citation Subset: IM |
Copyright Information:
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© 2010 The Authors. Clinical and Experimental Immunology © 2010 British Society for Immunology. |
Affiliation:
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Instituto de Leucemia Experimental (ILEX)-CONICET, Academia Nacional de Medicina, Buenos Aires, Argentina. barbararearte@yahoo.com.ar |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, CD / biosynthesis Cyclophosphamide / administration & dosage Deoxycytidine / administration & dosage, analogs & derivatives Forkhead Transcription Factors / biosynthesis Immunity, Cellular / drug effects Immunity, Humoral / drug effects Immunosuppression Immunosuppressive Agents / administration & dosage Lipopolysaccharides / administration & dosage Mice Mice, Inbred BALB C Mifepristone / administration & dosage*, pharmacology Receptors, Glucocorticoid / antagonists & inhibitors T-Lymphocytes / drug effects*, immunology, metabolism, pathology T-Lymphocytes, Regulatory / drug effects*, immunology, metabolism, pathology |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD; 0/Forkhead Transcription Factors; 0/Foxp3 protein, mouse; 0/Immunosuppressive Agents; 0/Lipopolysaccharides; 0/Receptors, Glucocorticoid; 103882-84-4/gemcitabine; 50-18-0/Cyclophosphamide; 84371-65-3/Mifepristone; 951-77-9/Deoxycytidine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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