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Updated: Aug 13, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Microvascular effects of oral interleukin-6 on ischemia/reperfusion in the murine small intestine
F M Rollwagen1, Y Y Li, N D Pacheco
1Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, USA. frollag@usuhs.mil
Abstract:
Oral administration of interleukin-6 (IL-6) has been shown to reduce hemorrhage-induced bacterial translocation from the gut in mice and rats. To examine the intestinal microvasculature, mice were given the electron-dense tracer horseradish peroxidase (HRP) after hemorrhage and IL-6 or vehicle administration. In normal mice and in those hemorrhaged and given IL-6, the electron-dense marker, administered intravenously, could be found in intestinal capillaries and between mucosal epithelial cells, suggesting that the microvasculature was patent. In mice given saline after shock, however, no marker was present in the gut, suggesting that the intestinal microvasculature was unable to deliver the marker to the epithelia. When mice were given HRP intralumenally (il) the tracer was able to penetrate between intestinal epithelial cells only in mice given vehicle after hemorrhage. This finding suggests that hemorrhaged mice were susceptible to sepsis and endotoxic shock from the leaky gut. In normal and IL-6-treated mice, the tracer was unable to pass from the lumen between mucosal epithelial cells, because the presence of an intact zonula occludens prevented passage. Functional studies supported the electron microscopy findings. Bacteria were cultured from the livers of mice fed vehicle after hemorrhage, but not from those fed IL-6. These data support the conclusions that parts of the intestinal microvasculature remain diminished after hemorrhage and resuscitation and that oral IL-6 restores this circulation.
Insights
Oral interleukin-6 (IL-6) administration in mice prevents gut barrier dysfunction after hemorrhage. This treatment preserves intestinal microvasculature integrity, reducing bacterial translocation and sepsis risk.
Area of Science:
- Gastroenterology
- Immunology
- Microcirculation Research
Background:
- Hemorrhage can lead to gut barrier dysfunction and bacterial translocation.
- Interleukin-6 (IL-6) has shown potential in mitigating these effects.
- The impact of IL-6 on intestinal microvasculature post-hemorrhage requires further investigation.
Purpose of the Study:
- To investigate the effect of oral interleukin-6 (IL-6) on intestinal microvasculature integrity following hemorrhage.
- To determine if IL-6 administration prevents increased intestinal permeability and bacterial translocation.
Main Methods:
- Mice underwent hemorrhage and received either IL-6 or vehicle orally.
- Intestinal microvasculature was examined using horseradish peroxidase (HRP) as an electron-dense tracer.
- Intestinal permeability was assessed by intralumenal HRP administration and bacterial cultures from liver tissue.
Main Results:
- Intravenous HRP reached intestinal capillaries and epithelial cells in normal and IL-6 treated mice, indicating patent microvasculature.
- Hemorrhaged mice receiving vehicle showed no HRP in the gut, suggesting compromised microcirculation.
- Intralumenal HRP penetrated epithelial cells only in vehicle-treated hemorrhaged mice, indicating a leaky gut.
- Bacteria were cultured from livers of vehicle-treated mice but not IL-6 treated mice.
Conclusions:
- Hemorrhage and resuscitation can impair intestinal microvasculature function.
- Oral IL-6 administration restores intestinal microcirculation and barrier integrity.
- IL-6 treatment effectively prevents bacterial translocation from the gut after hemorrhage.
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