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Polymorphonuclear cell-mediated phagocytosis and superoxide anion release in insulin-dependent diabetes mellitus
E Serlenga1, A R Garofalo, G De Pergola
1Department of Internal Medicine, University of Bari Medical Faculty, Italy.
Abstract:
It is well known that patients with insulin-dependent (or type I) diabetes mellitus are at high risk for bacterial infections. Since conflicting results have been reported on non-specific immune responses in type I diabetes, polymorphonuclear cell (PMN)-mediated phagocytosis and superoxide anion (O2-) generation in a group of individuals with well-controlled type I diabetes mellitus were assessed. Results showed that diabetic subjects were characterized by a significant impairment of phagocytic capacity when compared with healthy donors, while O2- release mimicked that seen in controls. Cell pretreatment with beta-hydroxybutyric acid (beta-HB) gave rise to a significant reduction in either phagocytosis or O2- production by PMN from type I diabetic individuals. Finally, beta-HB and glucose mixture supplementation to PMN suspensions did not induce any modification of their functional activities in comparison with those exerted by cells treated with beta-HB only. A disease-related or beta-HB-mediated PMN dysfunction in insulin-dependent diabetes mellitus is indicated.
Insights
Type 1 diabetes impairs polymorphonuclear cell (PMN) phagocytosis, increasing infection risk. Beta-hydroxybutyric acid (beta-HB) further reduces PMN function, suggesting a disease-related or beta-HB-mediated dysfunction in diabetic patients.
Area of Science:
- Immunology
- Endocrinology
- Diabetology
Background:
- Patients with insulin-dependent (type 1) diabetes mellitus face elevated risks of bacterial infections.
- Conflicting findings exist regarding non-specific immune responses in type 1 diabetes.
Purpose of the Study:
- To assess polymorphonuclear cell (PMN)-mediated phagocytosis and superoxide anion (O2-) generation in well-controlled type 1 diabetes mellitus patients.
- To investigate the impact of beta-hydroxybutyric acid (beta-HB) on PMN function in type 1 diabetes.
Main Methods:
- Assessed phagocytic capacity and O2- generation in PMNs from type 1 diabetic individuals and healthy controls.
- Examined the effect of beta-HB pretreatment on PMN function.
- Evaluated the combined effect of beta-HB and glucose on PMN activity.
Main Results:
- Diabetic subjects exhibited significantly impaired PMN phagocytic capacity compared to controls.
- O2- release by PMNs was comparable between diabetic and control groups.
- Beta-HB pretreatment significantly reduced both phagocytosis and O2- production in PMNs from type 1 diabetic individuals.
- Supplementation with a beta-HB and glucose mixture did not alter PMN function compared to beta-HB alone.
Conclusions:
- A disease-related or beta-hydroxybutyric acid-mediated dysfunction of PMNs is indicated in insulin-dependent diabetes mellitus.
- Impaired PMN phagocytosis may contribute to the increased susceptibility to infections in type 1 diabetes.
- Beta-HB's role in PMN dysfunction warrants further investigation in the context of diabetes.