Systemic Inflammatory Effects of Traumatic Brain Injury, Femur Fracture, and Shock: An Experimental Murine Polytrauma Model
Activation of the immune system for wound healing following accidental trauma is a well-studied phenomenon. The reaction comprises both the cellular and humoral systems. The various steps in the reaction are all temporally defined and influence each other. The main cells involved are polymorphonuclear granulocytes (PMN), monocytes, and lymphocytes. They interact and adhere to the endothelium via adhesion molecules such as L-selectin and ICAM-1. The humoral mediators discussed in this review are tumor necrosis factor-α (TNF-α) and its receptors, interleukin-1β (IL-1β), IL-6, IL-10 and interferon-γ (IFN-γ). The kinetics of the cells appearing and of the cytokines are discussed. The actions of these players are reviewed along with the most recent literature. Furthermore, we attempt to elucidate causal relationships. The immune system can be hyper- or hypoactive. Both exaggerated pro- and antiinflammatory reactions may have the same endpoint: multiple organ dysfunction syndrome (MODS). This knowledge should be used to meticulously monitor the patient’s immunologic status. Depending on the state, hyper- or hypoinflammatory, the treatment should comprise anti-inflammatory and immune-restoring properties, respectively. What is decisive to survival is timely, adequate management based on the individual patient’s status.