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Increased Autoreactivity of the Complement-Activating Molecule Mannan-Binding Lectin in a Type 1 Diabetes Model
Jakob Appel Østergaard1, Marieta Milkova Ruseva2, Talat Habib Malik2
1Department of Endocrinology and Internal Medicine, Aarhus University Hospital and Department of Clinical Medicine, Faculty of Health, Aarhus University, 8000 Aarhus, Denmark; The Danish Diabetes Academy, 5000 Odense, Denmark.
Journal of Diabetes Research
|March 16, 2016
Summary
Diabetic kidney disease involves increased mannan-binding lectin (MBL) in the kidneys, suggesting MBL plays a direct role in diabetic kidney complications and may be a new drug target.
Area of Science:
- Nephrology
- Immunology
- Diabetology
Background:
- Diabetic kidney disease is a leading cause of end-stage renal failure.
- The complement system, particularly mannan-binding lectin (MBL), is implicated in kidney prognosis.
- MBL activation in the diabetic glomerulus is hypothesized.
Purpose of the Study:
- To investigate MBL binding and complement activation in diabetic kidneys.
- To explore MBL's role in diabetic nephropathy.
Main Methods:
- Comparison of complement deposition in kidneys of diabetic and control mice.
- Immunofluorescence for MBL, C4, C3, and C9.
- Measurement of circulating complement activation product C3a.
Main Results:
- Glomerular MBL deposition significantly increased in diabetic mice.
- Circulating C3a levels were elevated in diabetic mice.
- No difference in glomerular C4, C3, or C9 deposition between groups.
Conclusions:
- Diabetes increases MBL autoreactivity in the kidney.
- Elevated circulating C3a suggests complement activation.
- Results support direct effects of MBL in the diabetic kidney.
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