Background
Kawasaki disease (KD) is an acute vasculitis in children, which ranks as the main cause of acquired heart disease in children in developed countries. The etiopathogenesis of KD remains to be clarified. Our study constructed a KD murine model and monitored the alterations of inflammatory factors and T cell subpopulations. Material/
Conclusions
Our findings reveal the characteristics of inflammatory factors and T cell subpopulations in CAWS-induced KD. Moreover, rhG-CSF might be an effective therapeutic regimen against KD.
Methods
Candida albicans cell wall extracts (CAWS) were utilized for inducing KD murine models. After 5 days, the mice were subcutaneously injected with rhG-CSF lasting 5 consecutive days. At 4 weeks, histopathology of hearts and arteries was observed via H&E staining. Inflammatory cytokine, chemokine, and adhesion molecule expression in serum specimens was detected via RT-qPCR and ELISA. T cell subpopulations in cardiac tissues were labeled through immunofluorescence and flow cytometry.
Results
CAWS induced cardiac dysfunction (reduced fraction shortening, increased left ventricle end-diastolic diameter and heart weight/body weight ratio) and cardiac and vascular inflammation, which were ameliorated by rhG-CSF treatment. CAWS-induced mice had increased levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), chemokine (RANTES), and adhesion molecules (MCP-1, VCAM-1, ICAM-1, E-selectin), as well as the decreased levels of anti-inflammatory cytokines (IL-10, G-CSF). Their levels were decreased following rhG-CSF administration. There were decreased CD3+, CD4+, CD8+, CD8+CD45+, Foxp3+, CD25+ and Foxp3+CD25+ T lymphocyte subpopulations and an increased CD45+ T lymphocyte subpopulation in cardiac tissues of CAWS-induced mice, which were ameliorated by rhG-CSF administration. Conclusions: Our findings reveal the characteristics of inflammatory factors and T cell subpopulations in CAWS-induced KD. Moreover, rhG-CSF might be an effective therapeutic regimen against KD.