Abstract
Bacterial translocation has been defined as the passage of viable bacteria through the epithelial mucosa and lamina propria of the gastrointestinal (GI) tract to extraintestinal sites such as the mesenteric lymph nodes (MLN), spleen, liver, peritoneum, and blood [1]. More recently, however, Alexander et al. [2] have suggested a refinement of this definition to include all microbial translocation (viable and nonviable) as well as microbial products, e.g., endotoxin, across an anatomically intact intestinal barrier. It should be noted that neither definition describes the host or bacterial mechanisms responsible for such movement. Currently, it is felt that indigenous bacteria translocate continuously from the GI tract. The numbers of bacteria that translocate are low and the host immune system is able to destroy them prior to systemic spread. This process may very well be a major mechanism of immune sampling to maintain “natural immunity” to a variety of pathogens. Thus, in the presence of normal GI ecology and a well-functioning immune system, the relative impermeability of the GI mucosa, “gut barrier function”, prevents invasion of bacteria into extraintestinal sites [3].
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Pasquale, M.D., Cipolle, M.D., Cerra, F.B. (1994). Bacterial Translocation: Myth versus Reality. In: Reinhart, K., Eyrich, K., Sprung, C. (eds) Sepsis. Update in Intensive Care and Emergency Medicine, vol 18. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85036-3_7
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