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Published on: September 15, 2017
MFG-E8 in Kawasaki Disease: Role in Endothelial Injury and Diagnostic Potential
Qiongfei Pei1,2,3, Jing Zhang1,2,3, Mengling Li1,2,3
1Department of Cardiovascular Medicine, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, People's Republic of China.
Insights
Milk Fat Globule Epidermal Growth Factor 8 (MFG-E8) is lower in children with Kawasaki disease (KD), particularly those with coronary artery lesions. MFG-E8 treatment reduced inflammation and cell damage in KD models.
Area of Science:
- Immunology
- Pediatric Cardiology
- Molecular Biology
Background:
- Kawasaki disease (KD) is a leading cause of acquired heart disease in children.
- Coronary artery lesions (CALs) are a severe complication of KD, occurring in non-responsive cases to standard therapy.
- Milk Fat Globule Epidermal Growth Factor 8 (MFG-E8) is an immune-modulating glycoprotein.
Purpose of the Study:
- To investigate the role of MFG-E8 in Kawasaki disease pathogenesis.
- To assess MFG-E8 as a potential diagnostic biomarker for KD.
- To evaluate the therapeutic potential of MFG-E8 in KD-associated vasculitis.
Main Methods:
- Serum MFG-E8 levels were quantified using ELISA in KD patients and controls.
- A murine model of coronary vasculitis was established and treated with MFG-E8.
- In vitro studies assessed MFG-E8's effects on endothelial cells exposed to KD serum, examining pyroptosis and oxidative stress.
Main Results:
- Serum MFG-E8 levels were significantly decreased in KD patients, especially those with CALs.
- MFG-E8 supplementation attenuated coronary vasculitis, reduced endothelial pyroptosis, and mitigated oxidative stress in vivo and in vitro.
- Combined analysis of MFG-E8, Fbg, and TT improved diagnostic accuracy for KD.
Conclusions:
- MFG-E8 shows promise as a diagnostic biomarker for Kawasaki disease.
- MFG-E8 demonstrates protective effects against endothelial injury in the acute phase of KD, suggesting therapeutic potential.
Background:
Kawasaki disease (KD) is a systemic vasculitis predominantly affecting children under five years old, with coronary artery lesions (CALs) being a severe complication. Despite the effectiveness of intravenous immunoglobulin (IVIG) therapy, a subset of patients remains unresponsive, necessitating alternative strategies. Milk Fat Globule Epidermal Growth Factor 8 (MFG-E8) is a secreted glycoprotein that functions as a bridge between damaged cells and phagocytes, conferring the ability to regulate immunity and inflammation. This study aimed to investigate the potential role of MFG-E8 in KD pathogenesis.
Methods:
Serum levels of MFG-E8 were measured via ELISA. CAWS was utilized to induce a murine model of coronary vasculitis, with MFG-E8 being administered intraperitoneally for treatment. Histological evaluation was conducted using H&E and IHC staining. Serum-stimulated THP-1 cells were co-cultured with endothelial cells to establish an inflammatory environment in vitro, with exogenous supplementation of MFG-E8. Pyroptosis-related markers were assessed by Western blot or immunofluorescence staining. Oxidative stress-related indicators were measured using commercially available assay kits.
Results:
Serum MFG-E8 levels were significantly lower in KD patients, especially those with CALs, compared to febrile and healthy controls. ROC analysis showed that combining MFG-E8 with Fbg and TT improved the ability to distinguish KD from other febrile illnesses. Further analyses displayed negative correlations between MFG-E8 and parameters pointing to inflammation. In the murine model of vasculitis, MFG-E8 supplementation alleviated coronary artery inflammation, reduced endothelial cell pyroptosis, and mitigated oxidative stress. Similar results were presented in vitro experiments using KD serum-treated endothelial cells.
Conclusion:
MFG-E8 represents a potential biomarker for the diagnosis of KD and exhibits protective effects against endothelial cell injury during the acute phase.
