Intestinal Cytokines

Abstract

The past two decades have witnessed the emergence of a new syndrome, named multiple organ failure (MOF), which today continues to represent the very first cause of death in critical care patients. In contrast to the spectacular advances made in the therapy of end-stage single organ failure patients, our inability to treat successfully acutely ill patients with MOF and to prevent the syndrome will be the major challenge for the end of this century [1–6]. Increasing numbers of investigators [1, 5, 7–16] have focused on the role of the gastrointestinal (GI) tract in the pathogenesis of this syndrome. The gut is now very often described as “the undrained abscess” or the “motor of MOF” [7]. Because it contains such a huge amount of bacteria and bacterial products, the gut has been very logically suspected to be the major source for the bacteremia that are often detected during the course of MOF [4, 7, 8]. Endotoxin translocation is also suspected to occur frequently during severe insults to the body, and it is an attractive concept to imagine that endotoxin coming from the digestive tract could play an important role in this setting. However, bacterial or even endotoxin translocation has not been demonstrated in humans and is far from being constant in all animal models of gut ischemia [17, 18]. Moreover, it is still possible to create a severe MOF in germ free animals [19]. Thus, the concept of “bacterial translocation (BT)“ remains highly controversial. On the other hand, high levels of a variety of cytokines have been described, not only in the systemic blood which is a very common finding in both animal models [20, 21] and in humans [22–24], but also in portal blood [23, 25, 26].