Novel model of peripheral tissue trauma-induced inflammation and gastrointestinal dysmotility.

摘要: Background  Trauma is a leading cause of death and although the gut recognized as ‘motor’ post-traumatic systemic inflammatory response syndrome multiple organ failure, studies on gastrointestinal (GI) tract are few. Our objectives were to create precisely controllable tissue injury model in which GI motility, inflammation wound fluid can be analyzed. Methods  A non-narcotic murine trauma was developed by subcutaneous dorsal trans-implantation devitalized donor syngeneic harvested tissue–bone matrix (TBX), adjusted % total body weight studied after 21 h. Gastrointestinal transit histograms plotted oral administration non-digestible FITC-dextran geometric centers calculated. Organ bath evaluated jejunal circular muscle contractility. Multiplex electrochemiluminescence measurements serum TBX mediators performed. Key Results  Increasing amounts progressively delayed transit, whereas heat denaturation or decellularization prevented ileus death. In TBX17.5% model, contractility suppressed significant elevations IL-6, keratinocyte cytokine IL-10 compared sham. addition, responses within showed elevated levels preformed IL-1β TNF-α, whereas, 21 h implantation IL-1β, IL-6 significantly increased wound. Conclusions & Inferences  novel that adjustable recapitulates important clinical phenomena. The demonstrated increasing caused ileus, initiated changes wound.