Related Experiment Videos
The effect of mesenteric lymphadenectomy and Kupffer cell depletion on bacterial translocation
Anders Stenbäck1, Staffan Meurling, Cristinel Cantar
1Department of Pediatric Surgery, University Hospital, Uppsala, Sweden.
Background:
Infectious complications are associated with high morbidity in patients with short bowel syndrome and after small bowel transplantation. Bacterial translocation from the intestine is probably an essential factor in the genesis of these infections. In a model for bacterial translocation in the rat we examined the consequence of mesenteric lymphadenectomy and the depletion of Kupffer cells.
Materials And Methods:
The effect of mesenteric lymphadenectomy was studied in two different models; in rats where a Thiry-Vella loop had been created from small bowel and in rats that had received a syngeneic small bowel transplant. To study the role of the Kupffer cells, rats with Thiry-Vella loops were treated intravenously with the Kupffer cell inhibitor gadolinium chloride. All animals were sacrificed on Day 3 postoperatively and the bacterial translocation to the mesenteric lymph nodes, liver, spleen, lung, and blood was evaluated.
Results:
Removal of the mesenteric lymph nodes did not result in any increased bacterial translocation in animals with a Thiry-Vella loop. However, the inactivation of Kupffer cells with gadolinium chloride produced a more severe translocation to the liver, spleen, and lungs. After small bowel transplantation the bacterial translocation to the spleen was increased in animals without mesenteric lymph nodes.
Conclusions:
In the model of bacterial translocation from a defunctionalized loop of small bowel the inhibition of Kupffer cells will promote the systemic spread of the translocating bacteria. This indicates an important protective function of the Kupffer cells against translocating microbes.
Insights
Kupffer cells, crucial immune cells in the liver, prevent bacteria from spreading throughout the body after intestinal surgery. Inhibiting these cells increases bacterial translocation, highlighting their protective role in short bowel syndrome and transplantation.
Area of Science:
- Gastroenterology
- Immunology
- Transplantation Surgery
Background:
- Infectious complications are a major concern in short bowel syndrome and small bowel transplantation.
- Bacterial translocation from the gut is a key factor in these infections.
- This study investigates the roles of mesenteric lymph nodes and Kupffer cells in bacterial translocation.
Purpose of the Study:
- To evaluate the impact of mesenteric lymphadenectomy on bacterial translocation.
- To determine the role of Kupffer cells in preventing systemic bacterial spread.
- To elucidate mechanisms of infection in short bowel syndrome and transplantation models.
Main Methods:
- Two rat models were used: Thiry-Vella loops and syngeneic small bowel transplants.
- Mesenteric lymphadenectomy was performed in separate groups.
- Kupffer cells were inactivated using gadolinium chloride in Thiry-Vella loop models.
- Bacterial translocation was assessed in lymph nodes, liver, spleen, lungs, and blood.
Main Results:
- Mesenteric lymphadenectomy did not increase bacterial translocation in Thiry-Vella loop models.
- Inactivation of Kupffer cells significantly increased bacterial translocation to the liver, spleen, and lungs.
- In small bowel transplant models, bacterial translocation to the spleen was elevated after lymphadenectomy.
Conclusions:
- Kupffer cells play a vital protective role against systemic spread of bacteria translocating from the intestine.
- Inhibition of Kupffer cells exacerbates bacterial translocation, underscoring their importance in maintaining gut barrier integrity.
- These findings have implications for managing infectious complications in patients with short bowel syndrome and undergoing small bowel transplantation.