- 作者: Miriam Neher; Sebastian Weckbach; Michael A Flierl; Markus S Huber-Lang and Philip F Stahel
- 作者服務機構: Department of Orthopaedic Surgery, University of Colorado Denver, School of Medicine, Denver Health Medical Center, Denver, CO, U.S.A.
- 中文摘要: --
- 英文摘要:
Trauma represents the leading cause of death among young people in industrialized
countries. Recent clinical and experimental studies have brought increasing evidence for
activation of the innate immune system in contributing to the pathogenesis of traumainduced
sequelae and adverse outcome. As the “first line of defense”, the complement
system represents a potent effector arm of innate immunity, and has been implicated in
mediating the early posttraumatic inflammatory response. Despite its generic beneficial
functions, including pathogen elimination and immediate response to danger signals,
complement activation may exert detrimental effects after trauma, in terms of mounting an
“innocent bystander” attack on host tissue. Posttraumatic ischemia/reperfusion injuries
represent the classic entity of complement-mediated tissue damage, adding to the
“antigenic load” by exacerbation of local and systemic inflammation and release of toxic
mediators. These pathophysiological sequelae have been shown to sustain the systemic
inflammatory response syndrome after major trauma, and can ultimately contribute to
remote organ injury and death. Numerous experimental models have been designed in
recent years with the aim of mimicking the inflammatory reaction after trauma and to allow
the testing of new pharmacological approaches, including the emergent concept of sitetargeted
complement inhibition. The present review provides an overview on the current
understanding of the cellular and molecular mechanisms of complement activation after
major trauma, with an emphasis of emerging therapeutic concepts which may provide the
rationale for a “bench-to-bedside” approach in the design of future pharmacological
strategies. - 中文關鍵字: --
- 英文關鍵字: --