ReviewCurrent theories on the pathophysiology of multiple organ failure after trauma
Introduction
The biological immune response to trauma is a host-defence response. The process of inflammatory reaction to trauma involves mediators (cytokines, chemokines, complement, oxygen radical, eicosanoid and nitric oxide (NO)) and effector cells (neutrophil, monocytes/macrophages and endothelial cells). All these factors are interrelated and interconnected by up-regulatory and down-regulatory mechanisms, which lead to systemic inflammatory response syndrome (SIRS). However, uncontrolled systemic inflammation and imbalance of the production of these inflammatory factors as the result of massive systemic immunological activation after severe trauma results in organ dysfunction. The level of immunological alteration which leads to SIRS in the wake of multiple organ failure (MOF) is regulated by the degree of injury, the type of injured tissue, age, sex, polymorphism and physical condition (exo- and endogenic factors). The purpose of this review is to highlight our current knowledge on the pathophysiology of MOF after trauma.
Section snippets
Cytokines
The cytokine response is an important factor in the development of SIRS; during SIRS, pro-inflammatory cytokines (IL-1, TNF-α, IL-6, IL-8, IL-12, IL-18, G-CSF and GM-CSF) are released excessively. With the release of pro-inflammatory cytokines during the initial phase of trauma anti-inflammatory cytokines, including IL-1Ra, IL-4, IL-10, IL-11 and IL-13 are released. The role of the anti-inflammatory cytokines is to down-regulate the production of pro-inflammatory cytokines. Normally, the
Conclusion
The pathogenesis of posttraumatic complications such as SIRS, ARDS and MOF remains incompletely understood. There have been numerous efforts to elucidate the mechanisms of SIRS, ARDS and MOF. These studies revealed that cells of the immune system (PMNs, lymphocytes, monocytes/macrophages, dendritic cells and endothelial cells) and the release of pro- and anti-inflammatory cytokines, chemokines, adhesion molecules, complement, protease, eicosanoids, ROS and NO are involved in these complications
Conflict of interest
There is no conflict of interest on our manuscript.
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