Microbial translocation and impairment of mucosal immunity induced by an elemental diet in rats is prevented by selective decontamination of the digestive tract.

OBJECTIVE

To assess the effect of selective decontamination of the digestive tract (SDD) on intestinal secretory immunoglobulin A (sIgA) concentrations in a model of intestinal bacterial overgrowth and bacterial translocation induced by an elemental diet in rats.

DESIGN

Laboratory study.

SETTING

University hospital, Germany.

MATERIAL

45 specific pathogen free female Crl:CD(R) BR rats.

INTERVENTIONS

For 7 days, 3 groups of rats were fed orally with standard chow (n = 15), total parenteral nutrition solution (ORAL-TPN, n = 15), or ORAL-TPN plus tobramycin (20 mg/L) and polymyxin E (25 mg/L) (ORAL-TPN + SDD).

MAIN OUTCOME MEASURES

Bacterial translocation to mesenteric lymph nodes (MLN), numbers of gram negative enterobacteria and total aerobic bacteria in the caecum, and intestinal concentrations of sIgA.

RESULTS

The incidence of bacterial translocation was significantly increased in the group given ORAL-TPN (8/15, 53%) compared with the group given chow (1/15, 7%, p < 0.01). Supplementation of ORAL-TPN with SDD reduced translocation to 0/15. The ORAL-TPN group had a pronounced overgrowth of aerobic bacteria in the caecum, mainly by gram negative enterobacteria, which was prevented by the SDD. The concentrations of intestinal sIgA were significantly reduced in the ORAL-TPN group. SDD resulted in both the soluble and insoluble sIgA fractions in the gut being within the reference ranges.

CONCLUSION

SDD prevents gram negative caecal overgrowth and translocation to MLN in rodents fed on ORAL-TPN. The significantly reduced mucosal immunity caused by ORAL-TPN alone is restored by SDD, although one might have expected a further reduction in sIgA concentrations with lower microbial populations than in the ORAL-TPN group. Not only does SDD not seem to affect the mucosa associated immune system adversely, but also depressed mucosal immunity was restored.