Oral-TPN-induced bacterial translocation and impaired immune defenses are reversed by refeeding.
Although certain defined diets have been shown to promote bacterial translocation (BT), the ability to reverse diet-induced BT has not previously been investigated. Furthermore, little is known about the effects of defined diets on host immune defenses. To address these questions, we measured BT and immune reactivity in rats fed a normal diet or enteral elemental (ORAL-TPN) diet. After 7 days on the elemental or normal diet, the rats were killed, and BT and mitogen responsiveness to concanavalin A and phytohemagglutinin were measured. In separate experiments, the effects of these diets on in vivo host defenses was measured with a Staphylococcus aureus abscess model. Additional experiments were performed to determine the time required to reverse ORAL-TPN-induced BT and impairment of host immune defenses by reinstituting normal feedings. Administration of the ORAL-TPN diet for 7 days was associated with BT to the mesenteric lymph node complex of all animals, decreased blastogenic response of blood and splenic lymphocytes to mitogens, and decreased ability to control an in vivo infectious challenge with S. aureus. Each of the derangements was reversed by the reinstitution of normal feedings. In summary, the enteral administration of an elemental diet for 7 days is associated with disruption of the gut microflora, BT, and the development of an immunocompromised state, all of which can be reversed by refeeding the animals a normal diet.
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Department of Surgery, Louisiana State University Medical Center, Shreveport, La 71130.
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D000704:Analysis of Variance; D000818:Animals; D018407:Bacterial Physiological Phenomena; D002432:Cecum / Q000382:microbiology; D002465:Cell Movement; D004750:Enteral Nutrition; D005260:Female; D005526:Food, Formulated; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D010289:Parenteral Nutrition, Total / Q000009:adverse effects*; D051381:Rats; D011919:Rats, Inbred Strains; D013203:Staphylococcal Infections / Q000209:etiology