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. 2006 May 20:1:15.
doi: 10.1186/1749-7922-1-15.

Trauma: the role of the innate immune system

F Hietbrink  1 , L Koenderman, Gt Rijkers, Lph Leenen
Affiliations

Trauma: the role of the innate immune system

F Hietbrink et al. World J Emerg Surg. .

Abstract

Immune dysfunction can provoke (multiple) organ failure in severely injured patients. This dysfunction manifests in two forms, which follow a biphasic pattern. During the first phase, in addition to the injury by trauma, organ damage is caused by the immune system during a systemic inflammatory response. During the second phase the patient is more susceptible for sepsis due to host defence failure (immune paralysis). The pathophysiological model outlined in this review encompasses etiological factors and the contribution of the innate immune system in the end organ damage. The etiological factors can be divided into intrinsic (genetic predisposition and physiological status) and extrinsic components (type of injury or "traumaload" and surgery or "intervention load"). Of all the factors, the intervention load is the only one which, can be altered by the attending emergency physician. Adjustment of the therapeutic approach and choice of the most appropriate treatment strategy can minimize the damage caused by the immune response and prevent the development of immunological paralysis. This review provides a pathophysiological basis for the damage control concept, in which a staged approach of surgery and post-traumatic immunomonitoring have become important aspects of the treatment protocol. The innate immune system is the main objective of immunomonitoring as it has the most prominent role in organ failure after trauma. Polymorphonuclear phagocytes and monocytes are the main effector-cells of the innate immune system in the processes that lead to organ failure. These cells are controlled by cytokines, chemokines, complement factors and specific tissue signals. The contribution of tissue barrier integrity and its interaction with the innate immune system is further evaluated.

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Figures

Figure 1
Figure 1
Biphasic model of organ failure. Depiction of the biphasic model of organ failure (MOF), originally coined by Moore[8]. The relative degree of immune activation is displayed on an arbitrary scale on the vertical axis. The horizontal axis indicates the time following trauma. When injury is sustained, a systemic pro-inflammatory response (SIRS) is evoked which can lead to the early version of MOF. At a later stage a compensatory anti-inflammatory response syndrome (CARS) or mixed antagonist response syndrome (MARS) can lead to immune paralysis and subsequently, the late form of organ failure.
Figure 2
Figure 2
Factors involved in the etiology of post-traumaticorgan failure. Shows the complex of factors, mediators and effectors involved in the development of organ failure. The endogenic factors (genetic predisposition and physical condition) form the basis for the susceptibility of a patient to post-traumatic organ failure. The sustained injury is seen as the first hit on the immune response and the "burden of surgery" is seen as the second hit, which can excacerbate the inflammatory reaction. The mediators stimulate the effectors which cause end-organ damage.
Figure 3
Figure 3
Innate immunity in tissue damage. Shows the relation between several important factors involved in the pathophysiology of organ failure after tissue injury. The figure is explained in detail in the article. C3a: Complement factor 3a; C5a: Complement factor 5a; O2-: Radical oxygen; MBL: Mannose binding lectin; C1q: Complement factor 1q
Figure 4
Figure 4
Relation between innate immunity and tissue factors following trauma. Shows the synergistic relation between the activation of the innate immune system and the loss of organ barrier functions. Both can act independently to promote organ failure, or when working together (synergize) induce clinical evident organ failure.
See this image and copyright information in PMC

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