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Members of the endogenous flora have become recognized as major pathogens in nosocomial infections, and the intestinal tract has become recognized as a major portal of entry for these pathogens. The English-language literature on this topic has been summarized and a working hypothesis devised describing a mechanism whereby intestinal bacteria can escape and cause systemic disease. It is postulated that the motile phagocyte ingests intestinal bacteria, transports them to extraintestinal sites, fails to accomplish intracellular killing, and then liberates the bacteria in the extraintestinal site. This hypothesis is consistent with many observations found in the literature: (1) The intestinal bacteria that most readily translocate out of the intestinal tract are classified as facultative intracellular pathogens. (2) Intestinal particles with no intrinsic motility (e.g., yeast, ferritin, starch) can translocate out of the intestinal lumen within hours after their ingestion. (3) The rate of translocation of intestinal bacteria can be altered with agents that modulate immune (including phagocytic) function. In the context of the mechanisms involved in intestinal immune responses, bacterial translocation appears to be a part of the normal antigen-sampling process of gut-associated lymphoid tissue. Systemic disease caused by translocating intestinal bacteria could be due to a maladaptation of the antigen-sampling process that has been designed to regulate the immune response to intestinal antigens.
Wells et al. (Thu,) studied this question.