IMPAIRED MOVEMENT AND DEFORMABILITY OF NEUTROPHILS FROM PATIENTS WITH JUVENILE DIABETES MELLITUS. AN INSULIN INDUCED DEFECT?

Abstract

Data from several laboratories have demonstrated deficient chemotaxis of polymorphonuclear leukocytes (PMNS) from subjects with insulin dependent juvenile diabetes mellitus (JOM). Me have also found deficient generation of antigen-antibody generated chemotactic activities from serums of patients with JDM. All patients previously studied were on insulin therapy at the time of study. In further exploring these relationships, we have added several new parameters: 1) Me have studied, over the past three years, 8 children with JDM prior to and following the institution of insulin therapy; and, 2) studied deformability of PMNS from JDM by the technique of elastimetry, which measures rigidity of the PMN membrane. The data show: 1) Before insulin, no defect in JDM PMN movement or generation of chemotactic activity from JDM serums could be demonstrated; 2) Following insulin, sometimes within 12-24 hours, highly significant (p < .001) decreases were found in both cellular and humoral chemotaxis; 3) Deformability of JDM PMNS was markedly decreased when chemotaxis was diminished. The data, therefore, strongly suggest that a PMN membrane alteration occurs following insulin therapy in JDM. This is consistent with recent studies demonstrating decreased adherence of JDM PMNS and may explain the apparent chemotactic defect.

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