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Microbial translocation and inflammatory response in patients with acute peritonitis
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Surgical Sciences.
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2004 In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, Vol. 39, no 7, 657-664 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2004. Vol. 39, no 7, 657-664 p.
Identifiers
URN: urn:nbn:se:uu:diva-92556OAI: oai:DiVA.org:uu-92556DiVA: diva2:165682
Available from: 2005-02-17 Created: 2005-02-17Bibliographically approved
In thesis
1. Inflammatory Reactions in Peritonitis and Malignant Obstructive Jaundice: Clinical and Experimental Studies with Special Emphasis on the Cellular Immune Response
Open this publication in new window or tab >>Inflammatory Reactions in Peritonitis and Malignant Obstructive Jaundice: Clinical and Experimental Studies with Special Emphasis on the Cellular Immune Response
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Patients with peritonitis or malignant obstructive jaundice (HPB+) have an increased morbidity and mortality due to sepsis. An altered cell-mediated immunity in the intestinal mucosa might promote gut barrier failure, increased endotoxin and cytokine release and bacterial translocation (BT) in these conditions. A clinically relevant rat model of polymicrobial peritonitis induced sepsis by cecal ligation and puncture (CLP) was used. Septic animals demonstrated a superficial injury in the small intestinal mucosa, and a significant reduction in T lymphocytes in the villi, as well as increased number of macrophages in the villi and in the MLNs as compared to sham. CLP caused increased concentration of TNF-α and IL-6 in ascitic fluid. CLP + the immunomodulator Linomide decreased the TNF-α level, reduced mucosal damage and attenuated the changes in T lymphocytes and macrophages observed following CLP. CLP + selective cyclooxygenase (COX)-2 inhibitor (SC-236) or nonselective COX inhibitor (indometacin) decreased the amount of macrophages in the mucosa and the MLNs compared to untreated CLP. CLP + indometacin decreased T lymphocytes in the villi and MLNs. SC-236 + CLP reduced mucosal injury and cytokine release as compared to indometacin. An increased rate of apoptosis in both the mucosa and MLNs was seen following CLP; COX inhibitors enhanced this phenomenon in the MLNs.

BT occurred infrequently in patients with acute peritonitis and in HPB+ there was no evidence of BT. Peritonitis and HPB+ causes significant inflammatory cellular reactions as increased endotoxin and cytokine plasma levels and an altered immune cell distribution in MLNs, in HPB+ a high rate of apoptosis in MLNs was observed.

An altered pattern of immunocompetent cells within the mucosa and in MLNs was found in experimental and clinical peritonitis as in HPB+. Lymphocyte depletion may be a result of increased apoptosis, which could reduce the ability of septic or jaundice patients to eradicate infection.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2005. 65 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 3
Keyword
Surgery, CLP, sepsis, peritonitis, bacterial translocation, malignant obstructive jaundice, Linomide, COX inhibitor, SC-236, indometacin, T lymphocyte, macrophage, mucosa, MLN, gut immune cell distribution, mucosal injury, cytokines, TNF-α, IL-6, IL-10, endotoxin, caspase-3, apoptosis, Kirurgi
National Category
Surgery
Identifiers
urn:nbn:se:uu:diva-4767 (URN)91-554-6138-7 (ISBN)
Public defence
2005-03-11, Auditorium Minor, Gustavianum, Akademigatan 3, Uppsala, 09:15
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Available from: 2005-02-17 Created: 2005-02-17Bibliographically approved

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