Innate immune response mechanisms in non-insulin dependent diabetes mellitus patients assessed by flow cytoenzymology

Citation
L. Llorente et al., Innate immune response mechanisms in non-insulin dependent diabetes mellitus patients assessed by flow cytoenzymology, IMMUNOL LET, 74(3), 2000, pp. 239-244
Citations number
25
Categorie Soggetti
Immunology
Journal title
IMMUNOLOGY LETTERS
ISSN journal
01652478 → ACNP
Volume
74
Issue
3
Year of publication
2000
Pages
239 - 244
Database
ISI
SICI code
0165-2478(20001101)74:3<239:IIRMIN>2.0.ZU;2-Q
Abstract
It is well known that infections in patients with diabetes mellitus are mor e severe, although there is controversy for increased susceptibility to the m. Non-specific immune response mechanisms could be related to defense and/ or susceptibility to pathogens. The aim of this study was to investigate th e activity of several enzymes involved in the primary host defense mechanis ms in non-insulin dependent diabetes mellitus (NIDDM). Twenty NIDDM females with a mean HbA(1c) level of 8.19% were included. No patient had clinical evidence of infection. As controls 20 healthy females were studied. The enz ymes tested were dipeptidylpeptidase I(DPP-I), cathepsin B and D, NADPH oxi dase and superoxide dismutase (oxidative burst) and collagenase. Isolated l eukocytes were incubated with the specific substrates in pyrogen free condi tions. The intracellular enzyme activity was analyzed by flow cytometry. Co llagenase enzymatic activity was similar in the three leukocyte subpopulati ons studied. Oxidative burst induction in monocytes was comparable between both groups. Enzyme activity of cathepsin B and D in all cell subsets, oxid ative burst in PMN cells, and DPP-I in lymphocytes and monocytes from patie nts, was higher than those from healthy females (P < 0.05). Overall, our fi ndings demonstrate an enhanced functional status of several intracellular l eukocyte enzymes in NIDDM. Furthermore, the increased oxidative burst induc tion and the consequent production of free radicals, may contribute to vasc ular complications. Other mechanisms - either from the non-specific or spec ific immune response - deserve investigation to establish if diabetic patie nts are more susceptible to infectious diseases. (C) 2000 Elsevier Science B.V. All rights reserved.