Elemental diet-induced bacterial translocation associated with systemic and intestinal immune suppression.
BACKGROUND
Elemental diets can lead to a loss of intestinal barrier function, promote bacterial translocation, and impair host immune defenses. The purpose of this study was to determine the effects of i.v. and orally administered total parenteral nutrition (TPN) solution on systemic and intestinal immunity and to establish whether supplemental cellulose fiber could improve the impaired immune response.


METHODS
The incidence of bacterial translocation and immune function was quantitated by measuring organ weights, immune cell population levels, and the mitogenic response of lymphocytes from the spleen, mesenteric lymph nodes and Peyer's patches of rats receiving parenteral or enteral TPN solution, 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 mitogens. Supplemental cellulose fiber reduced the incidence of diet-induced bacterial translocation from 84% to 31% (p < .01) and improved immune cell function. To more closely examine the relationship between bacterial translocation and impaired lymphocyte mitogenic activity, rats receiving TPN orally or i.v. were separated into two groups based on whether or not bacterial translocation occurred. Rats in which fiber prevented bacterial translocation had normal mitogenic responses, whereas the sub-group of rats in which fiber failed to prevent bacterial translocation had profound decreases in their lymphocyte mitogenic responses.


CONCLUSIONS
Both parenteral and enteral elemental diets induced bacterial translocation and impaired systemic and intestinal immune function. Fiber supplementation was effective in reducing elemental diet-induced bacterial translocation and significantly prevented diet-induced impairment of lymphocyte function.
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Department of Surgery, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103, USA.
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D000284:Administration, Oral; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D018988:Bacterial Translocation / Q000276:immunology / Q000502:physiology*; D001835:Body Weight; D015331:Cohort Studies; D004043:Dietary Fiber / Q000008:administration & dosage / Q000494:pharmacology*; D005526:Food, Formulated; D007262:Infusions, Intravenous; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology; D008099:Liver / Q000276:immunology / Q000502:physiology; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology / Q000382:microbiology; D008213:Lymphocyte Activation; D008297:Male; D008643:Mesentery; D009929:Organ Size; D010289:Parenteral Nutrition, Total / Q000009:adverse effects* / Q000379:methods; D010581:Peyer's Patches / Q000166:cytology / Q000276:immunology / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000166:cytology / Q000276:immunology / Q000502:physiology