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Extracellular histones are mediators of death through TLR2 and TLR4 in mouse fatal liver injury.

Xu, Jun; Zhang, Xiaomei; Monestier, Marc; Esmon, Naomi L; Esmon, Charles T.
J Immunol; 187(5): 2626-31, 2011 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-21784973
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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