| Popis: |
Infection remains the most common cause of postburn mortality in burn victims who survive the initial cardiopulmonary insult [35]. Infection is promoted by the loss of skin’s epithelial barrier and by a generalized postburn immunosuppression due to release of immunoactive agents from the burn wound [15]. Burn injury leads to suppression of nearly all aspects of the immune system [29]. Postburn serum levels of immunoglobulins, fibronectin, and complement are reduced, resulting in a diminished capacity for opsonization. Chemotaxis, phagocytosis, and the killing function of neutrophils, monocytes, and macrophages are impaired. Burn injury results in reductions in lymphocyte blastogenic response, cytotoxic ability, interleukin-2 (IL-2) production, and CD4/CD8 (helper/suppressor) cell ratio. Efforts at correcting this postburn immunosuppression using immunomodulators are increasingly being investigated [11, 17]. |
