The Role of DAMPS in Burns and Hemorrhagic Shock Immune Response: Pathophysiology and Clinical Issues. Review |
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Authors: | Desir Pantalone Carlo Bergamini Jacopo Martellucci Giovanni Alemanno Alessandro Bruscino Gherardo Maltinti Maximilian Sheiterle Riccardo Viligiardi Roberto Panconesi Tommaso Guagni Paolo Prosperi |
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Affiliation: | 1.ESA-European Space Agency Headquarter, 24 Rue de Général Bertrand, 75345 Paris, France;2.Department of Experimental and Clinical Medicine, University of Florence, 50121 Firenze, Italy;3.Trauma Team, Acute Care Surgery and Trauma Unit, Careggi University Hospital, Largo A. Brambilla 3, 50134 Florence, Italy; (C.B.); (J.M.); (G.A.); (A.B.); (G.M.); (M.S.); (R.V.); (R.P.); (T.G.); (P.P.) |
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Abstract: | Severe or major burns induce a pathophysiological, immune, and inflammatory response that can persist for a long time and affect morbidity and mortality. Severe burns are followed by a “hypermetabolic response”, an inflammatory process that can be extensive and become uncontrolled, leading to a generalized catabolic state and delayed healing. Catabolism causes the upregulation of inflammatory cells and innate immune markers in various organs, which may lead to multiorgan failure and death. Burns activate immune cells and cytokine production regulated by damage-associated molecular patterns (DAMPs). Trauma has similar injury-related immune responses, whereby DAMPs are massively released in musculoskeletal injuries and elicit widespread systemic inflammation. Hemorrhagic shock is the main cause of death in trauma. It is hypovolemic, and the consequence of volume loss and the speed of blood loss manifest immediately after injury. In burns, the shock becomes evident within the first 24 h and is hypovolemic-distributive due to the severely compromised regulation of tissue perfusion and oxygen delivery caused by capillary leakage, whereby fluids shift from the intravascular to the interstitial space. In this review, we compare the pathophysiological responses to burns and trauma including their associated clinical patterns. |
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Keywords: | burns DAMPs alarmin trauma cytokine production shock hemorrhagic shock |
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