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[The relationship between intestinal bifidobacteria and bacteria/endotoxin translocation in scalded rats]
Objective:
To investigate the potential role of intestinal bifidobacteria in the pathogenesis of gut-origin bacteria/endotoxin translocation in scalded rats.
Methods:
Wistar rats inflicted with 30% III degree scalding on the back were employed as the model with the rats undergoing sham injury as the control. The intestinal bacteria/endotoxin translocation and the changes in cecal mucosal microflora were determined by routine methods. And the plasma IL-6 concentration was measured with ELISA.
Results:
The incident of bacterial translocation into internal organs increased markedly in scalded rats (P = 0.001). The plasma LPS levels on 1, 3 and 5 postburn days (PBDs) in scalded rat group were much higher than those in sham injury group. The number of bifidobacteria decreased sharply 20 - 250 fold, the fungi increased 5 - 60 fold and E. coli increased 0.5 - 30 fold in the caecal mucosal microflora in the scalding group. The ratio of bifidobacteria to E. coli in the scalding group (4 - 800:1) was much lower than that in the sham injury group (25000:1). Furthermore, the plasma IL-6 level increased evidently in the scalding group. It was indicated by further analysis that compared with the rats without bacterial translocation, the bifidobacteria decreased 120 fold, the fungal number increased 50 fold and the E. coli number increased 30 fold in the scalded rats. The bifidobacterial number in the caecal mucosal microflora was negatively correlated with the plasma concentrations of IL-6 and LPS (P < 0.01) in the scalding rat group, and the plasma concentration of IL-6 was significantly and positively correlated with that of LPS.
Conclusion:
Severe scalding injury could lead to an the imbalance of intestinal microflora and the increased intestinal translocation of bacteria and LPS. The decrease of the ratio and number of bifidobacteria in the caecal mucosal microflora might be a contribute to the occurrence of postburn intestinal bacteria/endotoxin translocation.