Typical and atypical enteropathogenic Escherichia coli bacterial translocation associated with tissue hypoperfusion in rats.

Although enteropathogenic Escherichia coli (EPEC) are well-recognized diarrheal agents, their ability to translocate and cause extraintestinal alterations is not known. We investigated whether a typical EPEC (tEPEC) and an atypical EPEC (aEPEC) strain translocate and cause microcirculation injury under conditions of intestinal bacterial overgrowth. Bacterial translocation (BT) was induced in female Wistar-EPM rats (200-250 g) by oroduodenal catheterization and inoculation of 10 mL 10(10) colony forming unit (CFU)/mL, with the bacteria being confined between the duodenum and ileum with ligatures. After 2 h, mesenteric lymph nodes (MLN), liver and spleen were cultured for translocated bacteria and BT-related microcirculation changes were monitored in mesenteric and abdominal organs by intravital microscopy and laser Doppler flow, respectively. tEPEC (N = 11) and aEPEC (N = 11) were recovered from MLN (100%), spleen (36.4 and 45.5%), and liver (45.5 and 72.7%) of the animals, respectively. Recovery of the positive control E. coli R-6 (N = 6) was 100% for all compartments. Bacteria were not recovered from extraintestinal sites of controls inoculated with non-pathogenic E. coli strains HB101 (N = 6) and HS (N = 10), or saline. Mesenteric microcirculation injuries were detected with both EPEC strains, but only aEPEC was similar to E. coli R-6 with regard to systemic tissue hypoperfusion. In conclusion, overgrowth of certain aEPEC strains may lead to BT and impairment of the microcirculation in systemic organs.

Typical and atypical enteropathogenic Escherichia coli bacterial translocation associated with tissue hypoperfusion in rats

Although enteropathogenic Escherichia coli (EPEC) are well-recognized diarrheal agents, their ability to translocate and cause extraintestinal alterations is not known. We investigated whether a typical EPEC (tEPEC) and an atypical EPEC (aEPEC) strain translocate and cause microcirculation injury under conditions of intestinal bacterial overgrowth. Bacterial translocation (BT) was induced in female Wistar-EPM rats (200-250 g) by oroduodenal catheterization and inoculation of 10 mL 10(10) colony forming unit (CFU)/mL, with the bacteria being confined between the duodenum and ileum with ligatures. After 2 h, mesenteric lymph nodes (MLN), liver and spleen were cultured for translocated bacteria and BT-related microcirculation changes were monitored in mesenteric and abdominal organs by intravital microscopy and laser Doppler flow, respectively. tEPEC (N = 11) and aEPEC (N = 11) were recovered from MLN (100 percent), spleen (36.4 and 45.5 percent), and liver (45.5 and 72.7 percent) of the animals, respectively. Recovery of the positive control E. coli R-6 (N = 6) was 100 percent for all compartments. Bacteria were not recovered from extraintestinal sites of controls inoculated with non-pathogenic E. coli strains HB101 (N = 6) and HS (N = 10), or saline. Mesenteric microcirculation injuries were detected with both EPEC strains, but only aEPEC was similar to E. coli R-6 with regard to systemic tissue hypoperfusion. In conclusion, overgrowth of certain aEPEC strains may lead to BT and impairment of the microcirculation in systemic organs.

Can bacterial translocation be a beneficial event?

Infection is a major concern in intestinal transplant recipients. Bacterial migration to extraintestinal sites is a central component of the gut hypothesis of sepsis. However, some studies have cited the beneficial effects of bacterial translocation (BT) on the host acquired immune system. We evaluated the role of previous BT on a subsequent BT challenge, examined the BT index in organs as well as changes in white blood cell (WBC) count in mesenteric lymph and blood for correlation with outcomes. Wistar rats (n = 60) were divided into a BT group (n = 20), which underwent inoculation of 10 mL of 10(10) CFU/mL Escherichia coli R-6 confined to the small intestine as opposed to a BT1-14 group (n = 20), which underwent the BT procedure on days 1 and 14 or a S1-BT14 group (n = 20) that received 10 mL of saline on day 1 and the BT procedure on day 14. Half of the animals were killed 2 hours following the BT procedure. Samples from different compartments were collected for culture. Mesenteric lymph and peripheral blood were examined for WBC counts. The other half of the hosts was subjected to outcome evaluation concerning weight gain and mortality. Animals undergoing double BT showed a significantly lower index of bacterial recovery (liver, spleen, and blood) compared with those having a single BT (P < .05). The WBC count of mesenteric lymph cells after double BT was similar to naïve animals, but significantly lower than the single BT group (P < .05). The outcome was unchanged among double BT versus other groups. A previous BT challenge was efficient to generate a host-defense mechanism against a second BT episode induced by intestinal overgrowth with the same bacterial strain.

Bacterial translocation, microcirculation injury and sepsis.

Sepsis is the result from a complex bacterial-host interaction, which is an often-fatal response when host protective molecular mechanisms designed to fight invading bacteria surpass the beneficial intensity to the point of causing injury to the host. Increasing evidences have implicated the bacterial translocation (BT) as the main source for the induction of sepsis, although the beneficial effect of BT process has been related to the development of the intestinal immune response by physiological interaction between bacteria and host. In this article, we examined evolving concepts concerning to BT and discussed about its potential role in the promotion of microcirculation injury, moreover, its possible participation in the sepsis induction. According to our data obtained from in-vivo BT animal-model, both bacterial overgrowth and bacterial pathogenic determinants seem to be major predisposing factors for the induction of BT. Besides, translocation of luminal bacteria through the lymphatic via elicits the activation of the GALT inflammatory response contributing to microcirculation injuries, and the haematological via of BT was responsible to the systemic bacterial spread. On other hand, the combination of BT process to the pre-existing host systemic infection played a crucial role in the worsening of the clinical outcome. In our understanding, studies concerning to intestinal immune response and the pathophysiology of bacterial-host interaction, under normal and disease conditions, seems to be the key elements to the development of therapeutic approaches towards sepsis.