Cellular and humoral defense systems and inflammatory mechanisms in thermal injury.
Despite substantial improvements in modern burn care, sepsis is still a common feature in patients with severe thermal injury. Alterations in cell-mediated immunity, changes in inflammatory mediators and neutrophil functions, and recent data obtained from experimental studies in thermal injury are described.
D000818:Animals; D000917:Antibody Formation; D001770:Blood Bactericidal Activity; D002056:Burns / Q000097:blood / Q000150:complications / Q000276:immunology*; D002634:Chemotaxis, Leukocyte; D003170:Complement Pathway, Alternative; D003171:Complement Pathway, Classical; D006801:Humans; D007111:Immunity, Cellular; D007249:Inflammation / Q000097:blood / Q000276:immunology*; D008222:Lymphokines / Q000032:analysis / Q000096:biosynthesis; D009504:Neutrophils / Q000276:immunology / Q000502:physiology; D009895:Opsonin Proteins / Q000502:physiology; D010587:Phagocytosis; D011654:Pulmonary Edema / Q000209:etiology / Q000276:immunology / Q000503:physiopathology; D051381:Rats; D013491:Suppressor Factors, Immunologic
D008222:Lymphokines; D009895:Opsonin Proteins; D013491:Suppressor Factors, Immunologic