Effects of Prostaglandin E1 and E2 Analogues on Mucosal Injury-Induced, and on Bacterial Translocation Promoted by, Experimental Intestinal Obstruction

Abstract

The aim of this experimental study was to investigate effects of prostaglandin E1 and E2 analogues on mucosal structure and bacterial translocation during small bowel obstruction. The study was carried out on 40 Wistar rats equally divided into four groups; group 1 = control, group 2 = intestinal obstruction by ligation of distal ileum, and groups 3 and 4 = obstruction and administration of PGE2 and PGE1, respectively. Intestinal bacterial content and translocation to mesenteric lymph nodes and to the blood were determined by microbiological analysis. Mucosal structural changes were assessed by histopathological examination and expressed as a structural damage score and as the thickness of the mucosal layer. Bacterial overgrowth was determined in all obstruction groups. Mucosal thickness was 39.7 microm in group 1 and 26.8 microm in group 2 (p <.001). The thickness was significantly preserved by administration of PGE1 and PGE2 (p <.001). Mean structural damage score was 0.4 in group 1 and 6.7 in group 2 (p <.001). The damage scores were significantly lower in groups treated with PGE1 and PGE2 than obstruction alone group (p <.001). Better scores were obtained in rats treated with PGE1 than rats treated with PGE2 (p =.0026). Translocation to the lymph nodes did not occur in group 1, but was 70% in group 2 (p =.0015); significantly lower rates of translocation to lymph nodes were observed in rats treated with PGE1 (p =.035), but not with PGE2. We conclude that mucosal structure is partly maintained by administration of PGE1 and PGE2 during intestinal obstruction; PGE1 is more effective than PGE2 for ameliorating mucosal injury. PGE1 prevents bacterial translocation by preserving structural integrity of the mucosa. PGE2 partially prevents mucosal damage but not bacterial translocation.

The role of prostaglandin E2 (PGE 2) in toll-like receptor 4 (TLR4)-mediated colitis-associated neoplasia

“…When we used 16,16-dimethyl-PGE 2 either by i.p injection or gavage feeding (200 or 100 μg/150 μl/mouse, daily), all TLR4-/- mice succumbed during the active colitis period due to aggravated colitis (data not shown). Although PGE 2 has been implicated in intestinal cytoprotection against acute mucosal damage, overproduction or prolonged production of PGE 2 may worsen colitis or induce tumorigenesis, respectively [49-52]. Our results suggested that the balance of mucosal PGE 2 level to 15d-PGJ2 is important in determining the PGE 2 -mediated effect in the intestine.…”

The Effect of Caffeic Acid Phenethyl Ester on Bacterial Translocation and Intestinal Damage in Cholestatic Rats

“…In addition to causing primary disease, bacterial translocation may negatively affect the clinical course of some patients (15,16). Many experimental and clinical studies have confirmed the translocation of bacteria during bowel obstruction (17)(18)(19).…”

“…The mechanism of bacterial translocation is not completely understood. The alteration of enteric flora or physical or functional injury of the intestinal barrier can all induce bacterial translocation (18). Intestinal bacterial overgrowth can also cause intestinal oxidative damage.…”