| Novel model of peripheral tissue trauma-induced inflammation and gastrointestinal dysmotility. | |
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MedLine Citation:
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PMID: 21303433 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Trauma is a leading cause of death and although the gut is recognized as the 'motor' of post-traumatic systemic inflammatory response syndrome and multiple organ failure, studies on the gastrointestinal (GI) tract are few. Our objectives were to create a precisely controllable tissue injury model in which GI motility, systemic inflammation and wound fluid can be analyzed. METHODS: A non-narcotic murine trauma model was developed by the subcutaneous dorsal trans-implantation of a devitalized donor syngeneic harvested tissue-bone matrix (TBX), which was precisely adjusted to % total body weight and studied after 21 h. Gastrointestinal transit histograms were plotted after the oral administration of non-digestible FITC-dextran and geometric centers calculated. Organ bath evaluated jejunal circular muscle contractility. Multiplex electrochemiluminescence measurements of serum and TBX wound fluid inflammatory mediators were performed. KEY RESULTS: Increasing TBX amounts progressively delayed transit, whereas TBX heat denaturation or decellularization prevented ileus and death. In the TBX(17.5%) model, jejunal muscle contractility was suppressed and a systemic inflammatory response developed as significant serum elevations in IL-6, keratinocyte cytokine and IL-10 compared to sham. In addition, inflammatory responses within the wound fluid showed elevated levels of preformed IL-1β and TNF-α, whereas, 21 h after implantation IL-1β, IL-6 and keratinocyte cytokine were significantly increased in the wound. CONCLUSIONS & INFERENCES: A novel donor tissue-bone matrix trauma model was developed that is precisely adjustable and recapitulates important clinical phenomena. The non-narcotic model demonstrated that increasing tissue injury progressively caused ileus, initiated a systemic inflammatory response and developed inflammatory changes within the wound. |
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Authors:
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T Tsukamoto; V Antonic; I I El Hajj; A Stojadinovic; D G Binion; M J Izadjoo; H Yokota; H C Pape; A J Bauer |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-02-09 |
Journal Detail:
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Title: Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society Volume: 23 ISSN: 1365-2982 ISO Abbreviation: Neurogastroenterol. Motil. Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-05-31 Completed Date: 2011-10-11 Revised Date: 2012-04-04 |
Medline Journal Info:
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Nlm Unique ID: 9432572 Medline TA: Neurogastroenterol Motil Country: England |
Other Details:
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Languages: eng Pagination: 379-86, e164 Citation Subset: IM |
Copyright Information:
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© 2011 Blackwell Publishing Ltd. |
Affiliation:
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Department of Medicine/Gastroenterology, University of Pittsburgh, Pittsburgh, PA 15261, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bone Matrix / transplantation Gastrointestinal Diseases / blood, etiology*, physiopathology Gastrointestinal Motility / physiology* Inflammation / blood, etiology*, physiopathology Interleukin-10 / blood Interleukin-1beta / blood Interleukin-6 / blood Male Mice Mice, Inbred C57BL Models, Animal* Muscle Contraction / physiology Systemic Inflammatory Response Syndrome / blood, etiology*, physiopathology Tumor Necrosis Factor-alpha / blood Wounds and Injuries / complications* |
| Grant Support | |
ID/Acronym/Agency:
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DK02488/DK/NIDDK NIH HHS; P50-GM-53789/GM/NIGMS NIH HHS; R01 DK068610-05/DK/NIDDK NIH HHS; R01 GM058241-05/GM/NIGMS NIH HHS; R01 GM058241-09/GM/NIGMS NIH HHS; R01-DK068610/DK/NIDDK NIH HHS; R01-GM58241/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-1beta; 0/Interleukin-6; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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