The primary aim of this study was to clarify the mechanism and significance of lipopolysaccharide (LPS)-induced translocation of intestinal bacteria. Female Swiss Webster mice were purchased from two different animal suppliers. Twenty-four hours following parenteral LPS, mice from both suppliers had noticeable morbidity and mortality. However, intestinal pathology, gram-negative bacterial overgrowth, and increased bacterial translocation was noted in mice purchased from one supplier but not the other. Mice with increased translocation also had overgrowth of cecal gram- negative bacilli, i.e., 1010 per gram of cecum following parenteral LPS; in contrast, mice without LPS-induced bacterial translocation had 1,000- to 10,000-fold fewer cecal gram-negative bacilli. Additional groups of mice with increased bacterial translocation were also sacrificed two and 6 hr after parenteral LPS; morbidity and intestinal pathology were evident without a corresponding increase in bacterial translocation. Separate groups of these mice were also injected with platelet activating factor, resulting in intestinal pathology similar to that noted with parenteral LPS, but no increase in bacterial translocation. Thus parenteral LPS was consistently associated with morbidity and mortality but not with intestinal pathology, enteric bacterial overgrowth, or increased bacterial translocation.
|Original language||English (US)|
|Number of pages||7|
|State||Published - 1992|