Abstract

Impaired neutrophil chemotaxis has been consistently documented after thermal injury but whether this defect is primarily related to an acquired cellular defect or to humoral factors is not clear. To study this question, serial neutrophil chemotaxis measurements using the agarose technique of chemotaxis, were made in 34 patients with a mean burn size of 33%. Eighty-three percent of these patients developed a neutrophil chemotactic defect at some time during their hospital stay. The results of this study indicated that the serum from burn patients did not contain cell-directed inhibitor(s) of chemotaxis (CDI) or chemotactic factor inactivator(s). Furthermore, the chemotactic defect in the burn patient's neutrophils could not be reversed by normal human serum, suggesting that the cause of this defect was not related to the absence of normal circulating humoral substances. Additionally, no suppressive effect of silvadene (10 g/ml) on neutrophil chemotaxis was found. Therefore, we concluded that stable serum factors were not likely to play a major role in the development of the acquired neutrophil defect thermal injury.

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