ELEMENTAL DIET-INDUCED BACTERIAL TRANSLOCATION ASSOCIATED WITH SYSTEMIC AND INTESTINAL IMMUNE SUPPRESSION

Background: Elemental diets can lead to a loss of intestinal barrier f unction, promote bacterial translocation, and impair host immune defen ses. The purpose of this study was to determine the effects of IV and orally administered total parenteral nutrition (TPN) solution on syste mic and intestinal immunity and to establish whether supplemental cell ulose fiber could improve the impaired immune response. Methods: The i ncidence of bacterial translocation and immune function was quantitate d by measuring organ weights, immune cell population levels, and the m itogenic response of lymphocytes from the spleen, mesenteric lymph nod es and Peyer's patches of rats receiving parenteral or enteral TPN sol ution, with and without fiber supplementation. Results: Parenteral and enterally administered TPN solution promoted bacterial translocation to the mesenteric lymph nodes, reduced immune cell population levels, and decreased the lymphocyte mitogenic response to T- and B-cell mitog ens. Supplemental cellulose fiber reduced the incidence of diet-induce d bacterial translocation from 84% to 31% (p < .01) and improved immun e cell function. To more closely examine the relationship between bact erial translocation and impaired lymphocyte mitogenic activity, rats r eceiving TPN orally or IV were separated into two groups based on whet her or not bacterial translocation occurred. Rats in which fiber preve nted bacterial translocation had normal mitogenic responses, whereas t he subgroup of rats in which fiber failed to prevent bacterial translo cation had profound decreases in their lymphocyte mitogenic responses. Conclusions: Both parenteral and enteral elemental diets induced bact erial translocation and impaired systemic and intestinal immune functi on. Fiber supplementation was effective in reducing elemental diet-ind uced bacterial translocation and significantly prevented diet-induced impairment of lymphocyte function.