Emerging paradigm: toll-like receptor 4-sentinel for the detection of tissue damage.
The systemic inflammatory response syndrome initiated by infection shares many features in common with the trauma-induced systemic response. The toll-like receptors (TLRs) stand at the interface of innate immune activation in the settings of both infection and sterile injury by responding to a variety of microbial and endogenous ligands alike. Recently, a body of literature has evolved describing a key role for TLRs in acute injury using rodent models of hemorrhagic shock, ischemia and reperfusion, tissue trauma and wound repair, and various toxic exposures. This review will detail the observations implicating a TLR family member, TLR4, as a key component of the initial injury response.
Mollen
Kevin P
KP
Department of Surgery, University of Pittsburgh Medical Center, 200 Lothrop Street, Pittsburgh, PA 15213, USA.
Anand
Rahul J
RJ
Tsung
Allan
A
Prince
Jose M
JM
Levy
Ryan M
RM
Billiar
Timothy R
TR
D000818:Animals; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D007249:Inflammation / Q000276:immunology*; D008070:Lipopolysaccharides / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology; D012771:Shock, Hemorrhagic / Q000503:physiopathology; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000502:physiology*; D014945:Wound Healing / Q000502:physiology; D014947:Wounds and Injuries / Q000503:physiopathology*
D008070:Lipopolysaccharides; D051197:Toll-Like Receptor 4