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Abstract Data showing that bacterial translocation occurs are substantial, but it seems that the frequency with which translocation occurs in humans is much lower than that observed in animal models. Even more striking is the lack of strong data correlating bacterial translocation with clinically significant problems in humans. Still, extravagant postulations about the importance of bacterial translocation are continually being put forth in the literature. It seems that the hypothesis remains very attractive to researchers despite many studies that yielded weak correlative data. Bacterial translocation could indeed be a critical component to the development of SIRS, but human studies addressing the question are plagued by methodologic problems. Serial cultures of the mesenteric lymph nodes are not possible in human studies, so indirect methods will continue to be necessary tools. More frequent permeability studies and the use of more reliable and specific markers of bacterial translocation are urgently needed. Serial measurements of several proinflammatory and anti-inflammatory cytokines should be studied simultaneously, but studies such as these are very labor intensive. More studies should be undertaken in which tissue cytokine concentrations are measured, because these concentrations may be more relevant to disease states than are serum concentrations. Bacterial translocation may be a normal physiologic event without deleterious consequences. The baseline rate of translocation in most human studies is 5% to 10%. Berg stated that there is a normal rate in animals of approximately 10% to 20%. This may be a normal physiologic process by which animals sample different luminal antigens in order to produce immunocompetent cells. Bacterial translocation may occur as an innocent bystander. The vascular endothelium is injured after trauma and shock. Immune cells such as macrophages and infiltrating neutrophils become activated. Activated cells could engulf the bacteria normally found in mesenteric lymph nodes, carrying them to distant sites where they may cause disease. Recently, Vazquez-Torres et al. (Vazquez-torres et al., 1999) showed that Salmonella typhimurium can be carried from the intestinal lumen across the intestinal barrier and disseminated by invading CD18+ mucosal macrophages that routinely sample the lumen. Human studies have not yet assessed factors such as preexisting disease, age, sex, and host genetic factors that affect cytokine responses. When two patients have a similar insult, one may experience SIRS with a downward course, whereas the other may stabilize and recover. Host and genetic factors likely play an important role in these individual differences. Recently, genetic differences in cytokine responses have been documented in different human conditions. Severe rheumatoid arthritis, for example, has been associated with a 126-base pair allele related to a microsatellite polymorphism within the interferon γ gene. Increased hepatic fibrosis occurs in patients with hepatitis C who have certain high transforming growth factor β-producing genotypes (Powell et al., 2000). Finally, there is an association between interleukin 1 β polymorphism, Helicobacter pylori, and gastric cancer (El- Omar et al., 2000). Therefore, although bacterial translocation may increase after a variety of injuries, the complications of translocation and patient outcome may be more dependent on host factors than on the translocation itself. Theoretically, bacterial translocation may be modulated both quantitatively and qualitatively. Anumber of factors may be significance in modulating gut barrier function and consequently bacterial translocation in clinical practice. These act at pre-epithelial, epithelial and post- epithelial levels. It is recognized that these factors may act at more than one site, and indeed at more than one level. Probiotics, prebiotics, glutamine, curcumin and butyrate, are of the general preventive measures of bacterial translocation. |