Open AccessToll-Like Receptor 4 Mediates the Early Inflammatory Response After Cold Ischemia/Reperfusion
Author(s) -
David J. Kaczorowski,
Atsunori Nakao,
Kevin P. Mollen,
Raghuveer Vallabhaneni,
Ryujiro Sugimoto,
Junichi Kohmoto,
Kimimasa Tobita,
Brian S. Zuckerbraun,
Kenneth R. McCurry,
Noriko Murase,
Timothy R. Billiar
Publication year - 2007
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/01.tp.0000287597.87571.17
Subject(s) - tumor necrosis factor alpha , wild type , inflammation , tlr4 , reperfusion injury , biology , receptor , immunology , interleukin , hmgb1 , microbiology and biotechnology , cytokine , mutant , endocrinology , medicine , ischemia , biochemistry , gene
Ischemia/reperfusion (I/R) injury leads to graft dysfunction and may contribute to alloimmune responses posttransplantation. The molecular mechanisms of cold I/R injury are only partially characterized but may involve toll-like receptor (TLR)-4 activation by endogenous ligands. We tested the hypothesis that TLR4 mediates the early inflammatory response in the setting of cold I/R in a murine cardiac transplant model.