Selective translocation of coliform bacteria adhering to caecal epithelium of rats during catabolic stress

Abstract

Adult conventional rats were starved for 48 h with or without haemorrhage at 24 h, and translocation of caecal coliforms to mesenteric lymph nodes (MLNs) was measured. Translocation was detected in three of 11 rats without haemorrhage, in 6 of 11 starved and sham-operated rats and in 12 of 22 rats after haemorrhage. In contrast, only one of 13 non-instrumented and fed control rats showed translocation. Translocation was associated with more coliforms adhering to caecal epithelium in rats. Coliform isolates from caecum, caecal epithelium and MLNs were characterised and grouped into different biochemical phenotypes (BPTs) by a biochemical fingerprinting method. Of 291 BPTs detected in the caecum of all rats, 108 were also found on caecal epithelium; 36 BPTs were detected in MLNs, of which 17 were not detected either in the caecum or on the caecal epithelium of the corresponding rats. One isolate from each of these 36 BPTs was selected and compared to the others. Four common (C) BPTs (i.e., Cl-C4) were identified among them. Strains of C1 formed the majority of isolates from the caecum (79%), caecal epithelium (71%) and MLNs (91%). In contrast, C2-C4 had a significantly lower incidence both in the caecum and on the caecal epithelium, but not in the MLNs. These findings indicate that not all caecal coliforms adhere to the epithelium during catabolic stress and that for translocation to occur, other bacterial properties besides adhesion are needed. It is also concluded that coliforms with a low incidence in the caecum can translocate with the same efficiency as those with a high incidence.

Intestinal bacterial translocation in rats with cirrhosis is related to compromised paneth cell antimicrobial host defense

“…This shows the translocation of such marked bacteria from the gut to MLNs as well as into ascites fluid, representing the pathophysiological road for the development of spontaneous bacterial peritonitis in advanced cirrhosis. As described for other disease patterns that are accompanied by BT, e.g., intestinal obstruction, burn injury, or starvation, the translocation of almost exclusively coliform bacteria also underlines the pronounced preference of these gram‐negative strains to translocate 45, 46…”

Increased Type 1 Fimbrial Expression among CommensalEscherichia coliIsolates in the Murine Cecum following Catabolic Stress

“…Most of the studies examining the adherence of commensal gram-negative bacteria to the intestinal mucosa in vivo have been done in the rat model (20,28,35). In order to take advantage of available gene-targeted mouse lines in future studies, we developed a mouse model of catabolic stress involving partial hepatectomy, which results in increased energy demands due to tissue regeneration, and short-term starvation.…”

“…In the intestinal tract, while commensal bacteria are found to intimately colonize the mucosal surface, recent reports using molecular and immunohistochemical techniques have demonstrated that under normal conditions the mammalian intestinal epithelial cell surface is free of adherent bacteria (AB) (5,36). Nonetheless, commensal bacteria adhere to and translocate across the intestinal epithelium in association with a number of clinical situations, including hemorrhagic shock, immunosuppressive states, traumatic tissue injury, and lack of enteral feedings (4,6,15,20,28). Among the commensal bacteria, Escherichia coli in particular translocates efficiently across the intestinal epithelium in animal models and causes a large proportion of the septic episodes in critically ill patients, including patients with hepatic disease (6,25).…”

Pathogenesis of hepatic encephalopathy: the tumour necrosis factor-? theory

“…Indeed, haemorrhage, in general, from any organ, including the gastrointestinal tract, as a physical stress, stimulates TNF production and release [89]. Furthermore, gastrointestinal bleeding, specifically, causes increased incidence of bacterial infection [90], bacterial translocation [91], and systemic endotoxaemia [90,92]. These abnormalities, in turn, are strong stimulators for TNF production and release.…”