Thermal injury induce a two-phase inflammatory response: first, a pro-inflammatory status, resulting in a systemic inflammatory response syndrome, then an anti-inflammatory phase characterized by a profound defect in cellular-mediated immunity. This inflammatory reaction proceeds from complex phenomenons in whom many cellular elements are involved (macrophage is the central one) and very complex molecular products interact (especially cytokines). These phenomenons promote significant physiopathologic consequences, especially on cardiovascular homeostasis and endothelial permeability, that lower the prognosis. The inflammatory reaction can be modified, enhanced or maintained by adverse events (i.e. infection) resulting in degradation of clinical situation. Despite a better comprehension of the phenomenons underlying this inflammatory process, diagnosis or therapeutic applications are at that time disappointing.
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