The gut mesenteric lymph during bacterial translocation carries factor(s) related to mortality in sepsis

Introduction

Experimental and clinical studies have shown that bacterial translocation (BT) has been implicated in the pathogenesis of sepsis and multiple organ dysfunction syndrome (MODS). In this study we examined the role of the intestinal lymph during the BT process on the clinical outcome in a pre-established sepsis state.

Methods

Adult female Wistar rats (200–250 g) were submitted to the combination of induction of BT plus sepsis (S), with and without mesenteric lymph flow into the systemic circulation, and were monitored in terms of bacterial quantification per compartments and mortality (n = 20/each group). Groups: sepsis group (inoculation of 10⁷, 10⁹ or 10¹⁰ CFU/ml/100 g body weight of Enterobacter cloacae 89 into the portal vein); BT group (5 ml Escherichia coli R-6 10¹⁰ CFU/ml/100 g body weight confined to the small intestine for 2 hours); BT with lymphadenectomy group; and combination group (sepsis 10⁷ or 10⁹ plus BT-10¹⁰) with and without lymphadenectomy. The interruption of the lymph flow was achieved by mesenteric lymph node resection 5 days prior to the experiments, which is not a sufficient time for the re-canalization of the lymph ducts. The observation period for mortality was of 30 days in all groups.

Results

The BT groups and S-10⁷ group did not show any mortality; however, the combination of S-10⁷ or S-10⁹ with BT without lymphadenectomy significantly increased the mortality (50% within 32 hours and 100% within 13 hours, respectively) as compared with BT (0%), S-10⁷ (0%) and S-10⁹ (85% within 26 hours) alone. However, the combination group (S-10⁷ + BT-10¹⁰) with lymphadenectomy prevented death in all animals. In addition, the bacterial recovery in varying compartments of the combination groups was similar to the recovery of each group alone.

Conclusion

Overall data demonstrated significant deleterious synergistic effects of BT in combination with sepsis, suggesting that translocation of bacteria through the gut-associated lymphoid system might be the main factor for the aggravation of the host proinflammatory response. The BT process can thus be responsible for the installment of the MODS; moreover, this phenomena seems to not be related to the amount of translocated bacteria.