Cutting Edge: High-Mobility Group Box 1 Preconditioning Protects against Liver Ischemia-Reperfusion Injury
Author(s) -
Kunihiko Izuishi,
Allan Tsung,
Geetha Jeyabalan,
Nathan D. Critchlow,
Jianhua Li,
Kevin J. Tracey,
Richard DeMarco,
Michael T. Lotze,
Mitchell P. Fink,
David A. Geller,
Timothy R. Billiar
Publication year - 2006
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.176.12.7154
Subject(s) - hmgb1 , tlr4 , mediator , ischemic preconditioning , proinflammatory cytokine , reperfusion injury , ischemia , high mobility group , inflammation , sepsis , medicine , liver injury , pharmacology , chemistry , immunology , biochemistry , gene
High mobility group box 1 (HMGB1) is a NF released extracellularly as a late mediator of lethality in sepsis and as an early mediator of inflammation following injury. Here we demonstrate that in contrast to the proinflammatory role of HMGB1, preconditioning with HMGB1 results in protection following hepatic ischemia/reperfusion (I/R). Pretreatment of mice with HMGB1 significantly decreased liver damage after I/R. The protection observed in mice pretreated with HMGB1 was associated with a higher expression of IL-1R-associated kinase-M, a negative regulator of TLR4 signaling, compared with controls. We thus explored the possibility that HMGB1 preconditioning was mediated through TLR4 activation. HMGB1 preconditioning failed to provide protection in TLR4 mutant (C3H/HeJ) mice, but successfully reduced damage in TLR4 wild-type (C3H/HeOuj) mice. Our studies demonstrate that in contrast to the role of HMGB1 as an early mediator of inflammation and organ damage in hepatic I/R, HMGB1 preconditioning can be protective.
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