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T-cell inhibition does not aggravate bacterial translocation from rat small bowel
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Transplantation Surgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Paediatric Surgery.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Transplantation Surgery.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Paediatric Surgery.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Transplantation Surgery.
2006 (English)In: Transplant Immunology, ISSN 0966-3274, E-ISSN 1878-5492, Vol. 16, no 3-4, 208-214 p.Article in journal (Refereed) Published
Abstract [en]

Background: T-cell mediated immunity has been proposed to have an important function in the defence against translocating microbes from the gastrointestinal tract. After small bowel transplantation massive T-cell immunosuppression is necessary to avoid rejection. As a consequence, infections with intestinal bacteria are the main contributors to mortality in this setting. This could further imply that T cells are important in limiting bacterial translocation. In a model for bacterial translocation from small bowel in the rat we examined the outcome of T-cell inactivation. Methods: The studies were performed in a model of bacterial translocation from a Thiry-Vella loop of small bowel in the rat. The animals were treated with an anti-α/β T-cell receptor monoclonal antibody (R73). Inhibition of T-cell activation was also made using the immunosuppressive drug cyclosporin A. All animals were sacrificed on day 3 postoperatively and translocation to the mesenteric lymph nodes, liver, spleen, lung and blood was evaluated. Results: Treatment with R73 resulted in an almost complete labelling of T cells but did not result in any increased bacterial translocation compared to animals treated with saline. Neither did immunosuppression with cyclosporin A. Conclusions: In the model of bacterial translocation from a defunctionalised loop of small bowel the inhibition of T cells does not increase bacterial translocation to mesenteric lymph nodes or promote the systemic spread of the translocating bacteria. This indicates that T cells do not have any important protective function against translocating microbes from defunctionalised small bowel.

Place, publisher, year, edition, pages
2006. Vol. 16, no 3-4, 208-214 p.
Keyword [en]
Cyclosporin, Defunctionalised bowel, Mucosal barrier, R73, Small bowel transplantation, Thiry-Vella loop
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-93479DOI: 10.1016/j.trim.2006.09.024ISI: 000243241900010PubMedID: 17138055OAI: oai:DiVA.org:uu-93479DiVA: diva2:166965
Available from: 2005-09-15 Created: 2005-09-15 Last updated: 2015-06-15Bibliographically approved
In thesis
1. Studies of Experimental Bacterial Translocation
Open this publication in new window or tab >>Studies of Experimental Bacterial Translocation
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

One of the main obstacles to maintaining patients with short bowel syndrome on parenteral nutrition, or successfully transplanting these patients with a small bowel graft, is the many severe infections that occur. Evidence is accumulating that translocating bacteria from the patient’s bowel causes a significant part of these infections. In this thesis bacterial translocation is studied in a Thiry-Vella loop of defunctionalised small bowel in the rat.

Bacterial translocation to the mesenteric lymph nodes (MLNs) occurs in almost 100% of the rats after three days. No systemic spread of bacteria is observed unless there is additional immunosupression with depletion of Kupffer cells in the liver. However, blocking the function of α/β T cells does not increase the translocation. Removal of MLNs does not either aggravate bacterial translocation in the Thiry-Vella loop model. Conversely, after small bowel transplantation translocating bacteria spread systemically if the MLNs are removed.

The Thiry-Vella loop should also be a suitable model for the testing of potentially translocation-inhibiting substances. Reinforcement of the intestinal barrier with glutamine or phosphatidylcholine proved insufficient in decreasing bacterial translocation. Even selective bowel decontamination with tobramycin failed to abolish bacterial translocation. Thus, it seems that the driving force for translocation in this model is strong regardless of the relatively small trauma of intestinal defunctionalisation.

Flow cytometric studies of the immune cells in the spleen MLNs showed a decrease in MHC class II positive T cells in the MLNs of the Thiry-Vella loop. Concurrently the number of macrophages increased with time as observed by immunohistochemistry. The fraction of MHC class II negative macrophages increased in the spleens of rats treated with glutamine.

In conclusion, the Thiry-Vella loop model offers possibilities of immunological as well as mechanistic studies on bacterial translocation from small intestine.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2005. 60 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 71
Keyword
Surgery, Intestinal barrier, short bowel syndrome, small bowel transplantation, mesenteric lymph nodes, gadolinium chloride, T cell inactivation, glutamine, phosphatidylcholine, rat, Thiry-Vella loop, Kirurgi
National Category
Surgery
Identifiers
urn:nbn:se:uu:diva-5933 (URN)91-554-6339-8 (ISBN)
Public defence
2005-10-07, Rosénsalen, Akademiska Barnsjukhuset, Ing 95 NB, 751 85 Uppsala, 13:15
Opponent
Supervisors
Available from: 2005-09-15 Created: 2005-09-15 Last updated: 2011-02-18Bibliographically approved

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Stenbäck, AndersLorant, TomasJohnsson, Cecilia

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