Failure of local immunity. A potential cause of burn wound sepsis.
Destruction of the skin barrier by thermal injury removes the major local defense barrier to bacteria. To determine whether a local defect in immunity also existed, the opsonic activity of blister fluid against Staphylococcus aureus and Pseudomonas aeruginosa as well as neutrophil chemotaxis were measured. The results of these studies indicated that blister fluid could not opsonize Pseudomonas. A series of repletion experiments indicated that the opsonic defect for Pseudomonas was not due to the presence of inhibitors but was due to the lack of normal serum factor(s). Although both the level of immunoglobulins and complement components in the blister fluid was depressed, the cause of the opsoninopathy appeared to be due to local consumption of complement in the burn wounds. In addition to the opsoninopathy, both neutrophil chemotaxis and random migration were also depressed. In conclusion, a burn injury appears to cause severe impairment of both cellular and humoral local immunity, which could predispose these patients to burn wound sepsis.
D000293:Adolescent; D000328:Adult; D002056:Burns / Q000276:immunology*; D002634:Chemotaxis, Leukocyte; D003167:Complement Activation; D003176:Complement C3 / Q000032:analysis; D003179:Complement C3b / Q000032:analysis; D015933:Complement C3d; D005122:Exudates and Transudates / Q000276:immunology; D005260:Female; D006801:Humans; D007109:Immunity; D007136:Immunoglobulins / Q000032:analysis; D008297:Male; D009504:Neutrophils; D009895:Opsonin Proteins / Q000276:immunology; D010587:Phagocytosis; D011550:Pseudomonas aeruginosa; D013211:Staphylococcus aureus; D014946:Wound Infection / Q000276:immunology*
D003176:Complement C3; D007136:Immunoglobulins; D009895:Opsonin Proteins; D003179:Complement C3b; D015933:Complement C3d