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Sepsis provokes host's microbiota overgrowth of commensal Gram-negative bacteria and subsequent induction of bacterial translocation in rats


The literature has shown the participation of intestinal microbiota in the genesis of primary infections as well as of sepsis. In this study we examine the role of sepsis on the microbiota by examining the most frequently recovered Gram-negative bacteria (G-).

Materials and methods

Adult Wistar rats (± 200 g) were submitted to the induction of semi-lethal sepsis (S-G) (E. coli R6 1 ml of 108 CFU/ml/100 g body weight, i.v.). Firstly, fecal G – kinetic following sepsis induction was examined (6, 12, 24, 48, 72, 120 and 216 hours) (n = 6). After sepsis induction, in other groups (n = 18), samples were harvested from the small bowel (duodenum, jejunum, ileum) and large bowel (cecum and feces before and after sepsis) at 6, 12 and 24 hours, and the BT index was examined at the mesenteric lymph nodes (MLN), liver and spleen by culture in MacConkey medium. Control groups were the sham group (Sham-G, saline injection) (n = 18) and the naïve group (N-G, without any procedure) (n = 6).


Overall data showed that, after sepsis induction, fecal G – microbiota increased progressively up to 24 hours (P < 0.05) returning to control level after 72 hours (data not shown). Gut segment overgrowth was also found until 24 hours and BT occurred during this period (Figure 1).

Figure 1

Intestinal microbiota kinetic of sepsis vs controls and BT index. *P < 0.05.


Sepsis provoked G – overgrowth and this was able to induce the BT process. Other factors, such as splanchnic hypoperfusion, decreased peristalsis and gut immunity by sepsis, might have also contributed to this event.

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  • Small Bowel
  • Emergency Medicine
  • Sham Group
  • Large Bowel
  • Primary Infection