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Published on: August 12, 2016
Inhibition of polymorphonuclear leukocyte respiratory burst by elevated glucose concentrations in vitro
1Research Unit, Veterans Administration Medical Center, Boise, Idaho 83702.
Abstract:
Although impaired polymorphonuclear leukocyte (PMN) function may be a cause of infectious complications in diabetic patients, the mechanisms of altered cell function are not understood. Our studies of PMN function in healthy subjects demonstrated significant reduction in the respiratory burst after 30 min of in vitro cell exposure to glucose concentrations greater than 11 mM (200 mg/dl). The respiratory burst was reduced 28 +/- 5 and 74 +/- 7% in PMNs incubated with 11 and 56 mM glucose, respectively. The impairment was independent of the cell stimulus (chemotactic peptide, calcium ionophore, or phorbol ester) and was not affected by sorbinil or myo-inositol. Because both D- and L-glucose had similar inhibitory effects, a nonenzymatic mechanism appeared to be the cause of impaired PMN function. Although mannitol and sorbitol did not affect cell function, monosaccharides (glucose, mannose, fructose) that form Schiff-base adducts with protein inhibited PMN function. These findings suggest a potential role for protein glycosylation in glucose-induced impairment of PMN function.
Insights
High glucose levels impair polymorphonuclear leukocyte (PMN) function by reducing the respiratory burst. This suggests protein glycosylation may underlie glucose-induced PMN dysfunction in diabetes.
Area of Science:
- Immunology
- Metabolic Disorders
- Cellular Biology
Background:
- Diabetic patients often experience infectious complications.
- Impaired polymorphonuclear leukocyte (PMN) function is implicated in these complications.
- The precise mechanisms behind altered PMN function in diabetes remain unclear.
Purpose of the Study:
- To investigate the impact of glucose on PMN function.
- To elucidate the mechanisms of glucose-induced PMN impairment.
- To explore the role of protein glycosylation in this process.
Main Methods:
- Incubation of PMNs from healthy subjects with varying glucose concentrations (in vitro).
- Assessment of PMN respiratory burst activity using different stimuli.
- Evaluation of the effects of sorbinil, myo-inositol, mannitol, sorbitol, and other monosaccharides.
Main Results:
- Glucose concentrations above 11 mM significantly reduced PMN respiratory burst.
- Impairment was dose-dependent, with 56 mM glucose causing a 74% reduction.
- The effect was independent of the stimulus and not mediated by sorbinil or myo-inositol.
- Both D- and L-glucose inhibited function, suggesting a nonenzymatic mechanism.
- Monosaccharides forming Schiff-base adducts with proteins inhibited PMN function.
Conclusions:
- High glucose levels impair PMN respiratory burst function.
- Protein glycosylation is a likely mechanism for glucose-induced PMN dysfunction.
- These findings highlight a potential cellular basis for increased infection risk in diabetes.
