The intestinal hypothesis of sepsis has been attributed to bacterial translocation (BT), and the aggravation of sepsis is related to the increased vascular permeability state that potentates the BT index. In this study we examined the BT index during sepsis with or without mesenteric lymph exclusion.

Wistar rats (± 200 g) were submitted to the BT process (E. coli R6 10 ml of 10¹⁰ CFU/ml) and nonlethal sepsis (E. cloacae 89 2 ml of 10⁷ CFU/ml) plus BT, with or without mesenteric lymph interruption by mesenteric lymph node resection and lymph duct ligature 5 days prior to the experiments. Samples (blood, spleen and liver) were collected 2 hours after the innoculation and cultured to recover bacteria of intestinal origin. One-half of the animals per group was observed to mortality. Groups (n = 20/group): BT group (BT-G), BT with lymphadenectomy group (BTL-G), combination group (C-G) and combination with lymphadenectomy group (CL-G).

BT was 100% positive in all groups. The BT index was similar between the BT-G, the BTL-G and the CL-G (P = 0.6), and mortality was not observed in these groups although a considerable amount of translocated bacteria could be recovered, particularly at the liver and spleen (Figure 1). When BT was added to the sepsis without lymph exclusion (C-G), the BT index was statistically lower (P = 0.04); however, 50% (LD₅₀) of mortality occurred within 30 hours (Figure 1).

These results show that, more than the amount of translocated bacteria, the gut-associated lymphoid system activation by the BT process played a pivotal role in the worsening of sepsis. Besides, BT occurred independently of mesenteric lymph interruption, showing that the hematological route of BT might be the principal route for bacterial dissemination into the bloodstream.