| Extracellular Histones Are Mediators of Death through TLR2 and TLR4 in Mouse Fatal Liver Injury. | |
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MedLine Citation:
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PMID: 21784973 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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We previously reported that extracellular histones are major mediators of death in sepsis. Infusion of extracellular histones leads to increased cytokine levels. Histones activate TLR2 and TLR4 in a process that is enhanced by binding to DNA. Activation of TLR4 is responsible for the histone-dependent increase in cytokine levels. To study the impact of histone release on pathology we used two models: a Con A-triggered activation of T cells to mimic sterile inflammation, and acetaminophen to model drug-induced tissue toxicity. Histones were released in both models and anti-histone Abs were protective. TLR2- or TLR4-null mice were also protected. These studies imply that histone release contributes to death in inflammatory injury and in chemical-induced cellular injury, both of which are mediated in part through the TLRs. |
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Authors:
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Jun Xu; Xiaomei Zhang; Marc Monestier; Naomi L Esmon; Charles T Esmon |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-7-22 |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: - ISSN: 1550-6606 ISO Abbreviation: - Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-7-25 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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