Evidence of Polymorphonuclear Neutrophils (PMN) Activation in Patients With Insulin‐Dependent Diabetes Mellitus

Polymorphonuclear neutrophils' chemotaxis, surface charge, superoxide anions generation, NBT (nitro blue tetrazolium) reduction and intracellular lysozyme, and β‐glucuronidase content were estimated in patients with type I diabetes mellitus in a similar state of metabolic control. The chemotaxis of diabetic cells toward bacterial chemotactic factors was similar to controls, whereas migration toward complement‐derived chemoattractants was significantly reduced. Polymorphonuclear neutrophils isolated from diabetic patients, when unstimulated, produced significantly greater amounts of superoxide anions and reduced NBT more efficiently. They also revealed reduced surface charge and lower intracellular content of lysozyme, whereas β‐glucuronidase content was similar to controls. The results obtained seem to indicate that neutrophils in patients with insulin‐dependent diabetes manifest signs of being in the activated state. The possible mechanisms of such stimulation are discussed.

[1]  P. Ward.  Leukotactic factors in health and disease. , 1971, American Journal of Pathology.

[2]  W. Fishman,et al.  Chromogenic substrates; phenolphthalein glucuronic acid as substrate for the assay of glucuronidase activity. , 1946, The Journal of biological chemistry.

[3]  A. Dalmasso,et al.  Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes. , 1977, The Journal of clinical investigation.

[4]  Perillie Pe,et al.  Studies of the resistance to infection in diabetes mellitus: local exudative cellular response. , 1962 .

[5]  M. Schwartz,et al.  Effect of alcohol and various diseases on leukocyte mobilization, phagocytosis and intracellular bacterial killing. , 1970, The New England journal of medicine.

[6]  H. H. Balch,et al.  Blood bactericidal studies and serum complement in diabetic patients. , 1963, The Journal of surgical research.

[7]  M. D. Armstrong,et al.  THE PHAGOCYTIC ACTIVITY OF POLYMORPHONUCLEAR LEUKOCYTES OBTAINED FROM PATIENTS WITH DIABETES MELLITUS. , 1964 .

[8]  J. Nolan,et al.  Studies of the resistance to infection in diabetes mellitus: local exudative cellular response. , 1962, The Journal of laboratory and clinical medicine.

[9]  M. Miller,et al.  Leukocyte functions in juvenile diabetes mellitus: humoral and cellular aspects. , 1972, The Journal of pediatrics.

[10]  C. M. Macfarlane.  Secondary changes in diabetes mellitus with particular reference to retinopathy and neuropathy. , 1985, Medical hypotheses.

[11]  J. Repine,et al.  Bactericidal function of neutrophils from patients with acute bacterial infections and from diabetics. , 1980, The Journal of infectious diseases.

[12]  R. Matz,et al.  Adult Respiratory Distress Syndrome Complicating Severely Uncontrolled Diabetes Mellitus: Report of Nine Cases and a Review of the Literature , 1982, Diabetes Care.

[13]  B. Babior.  Oxidants from phagocytes: agents of defense and destruction. , 1984, Blood.

[14]  V. Esmann.  The polymorphonuclear leukocyte in diabetes , 1982 .

[15]  P. Dri,et al.  The measurement of superoxide anion production by granulocytes in whole blood. A clinical test for the evaluation of phagocyte function and serum opsonic capacity , 1983, European journal of clinical investigation.

[16]  H. Repo.  Leukocyte Migration Agarose Test for the Assessment of Human Neutrophil Chemotaxis , 1977, Scandinavian journal of immunology.

[17]  K. Suntharalingam,et al.  Diabetes and Neutrophil Chemotaxis , 1977, Diabetes.

[18]  M. Lichtman,et al.  Electrophoretic mobility and N-acetyl neuraminic acid content of human normal and leukemic lymphocytes and granulocytes. , 1970, Blood.

[19]  R. Weinsier,et al.  Death resulting from overzealous total parenteral nutrition: the refeeding syndrome revisited. , 1981, The American journal of clinical nutrition.

[20]  J. Bagdade,et al.  Impaired Leukocyte Function in Patients with Poorly Controlled Diabetes , 1974, Diabetes.

[21]  A. Wykrętowicz,et al.  Phagocytosis, bactericidal capacity, and superoxide anion (O2-) production by polymorphonuclear neutrophils from patients with diabetes mellitus. , 1985, Folia haematologica.

[22]  G. Keusch,et al.  Infection and diabetes: the case for glucose control. , 1982, The American journal of medicine.

[23]  J. Lunec,et al.  Fluorescence changes in human gamma-globulin induced by free-radical activity. , 1983, Biochimica et biophysica acta.

[24]  S. E. Hartsell,et al.  THE DETERMINATION OF LYSOZYME , 1949, Journal of bacteriology.

[25]  A Mowat,et al.  Chemotaxis of polymorphonuclear leukocytes from patients with diabetes mellitus. , 1971, The New England journal of medicine.

[26]  R. Simmons,et al.  Chemotactic deactivation of human neutrophils: evidence for nonspecific and specific components , 1978, Infection and immunity.

[27]  C. M. Nolan,et al.  Further Characterization of the Impaired Bactericidal Function of Granulocytes in Patients with Poorly Controlled Diabetes , 1978, Diabetes.

[28]  J. McCord,et al.  Free radicals and inflammation: superoxide-dependent activation of a neutrophil chemotactic factor in plasma. , 1980, Proceedings of the National Academy of Sciences of the United States of America.

[29]  G. Weissmann.  Activation of neutrophils and the lesions of rheumatoid arthritis. , 1982, The Journal of laboratory and clinical medicine.

[30]  J. Wallin,et al.  Chemiluminescence and superoxide anion production by leukocytes from diabetic patients. , 1983, The Journal of clinical endocrinology and metabolism.

[31]  B. Buckingham,et al.  Complement activation in type 1 human diabetes. , 1985, Clinical immunology and immunopathology.

[32]  J. Gallin,et al.  A functional differentiation of human neutrophil granules: generation of C5a by a specific (secondary) granule product and inactivation of C5a by azurophil (primary) granule products. , 1977, Journal of immunology.