Role of estradiol on intestinal permeability and bacterial translocation during systemic inflammation in female rats

The intestinal epithelium exerts a critical role as a barrier to prevent the dissemination of microorganisms from the gut. The integrity of this epithelium may be compromised during systemic inflammation, increasing intestinal permeability. The inflammatory mediators produced during systemic inflammation mediates the intestinal barrier disruption. Estradiol has been demonstrated as an anti-inflammatory hormone and responsible for maintaining the architecture of intestinal epithelium. In present study, we evaluated the role of estradiol on the intestinal permeability and bacterial translocation during systemic inflammation induced by lipopolysaccharide administration (LPS; 1.5 mg/kg, intravenous) in female rats. The female rats were ovariectomized and allowed to recover for 10-12 days before the experiment. For three consecutive days, rats were pre-treated with estradiol cypionate (50 or 100 µg/kg, subcutaneous) or corn oil (vehicle). The intestinal permeability was determined at 6h after LPS or saline administration by injecting FITC-dextran 4 kDa in the colon or ileum. Furthermore, the bacterial translocation was evaluated by the number of colony forming units in the mesenteric lymph nodes also at 6h after LPS administered. Our results demonstrate that estradiol reduces intestinal permeability in both gut segments, colon and ileum. Moreover, estradiol also prevents the bacterial translocation induced by LPS. This study suggests that estradiol participates in the gut protection against the deleterious effects of systemic inflammation on the intestinal epithelium.