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Lactobacillus plantarum CCFM639 ameliorates vascular dysfunction in mice with Kawasaki disease involving eNOS/NO
Fan Yu1, Teng Yang1, Yanyan Zhou1
1Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Insights
Lactobacillus plantarum CCFM639 effectively reduced inflammation and improved vascular and intestinal barrier function in a mouse model of Kawasaki disease (KD), offering a potential therapeutic strategy for pediatric vasculitis.
Area of Science:
- Microbiology
- Immunology
- Cardiovascular Research
Background:
- Kawasaki disease (KD) is a critical pediatric inflammatory condition affecting blood vessels, frequently leading to coronary artery complications and non-congenital heart issues.
- KD is the leading cause of acquired pediatric heart disease, necessitating novel therapeutic approaches.
Purpose of the Study:
- To investigate the therapeutic potential of Lactobacillus plantarum CCFM639 in mitigating systemic and vascular inflammation in a Kawasaki disease mouse model.
- To assess the impact of CCFM639 on intestinal barrier integrity and endothelial cell function.
Main Methods:
- Administration of Lactobacillus plantarum CCFM639 in a KD mouse model.
- Evaluation of systemic inflammation via spleen index and inflammatory cytokine levels.
- Assessment of vascular inflammation through histopathology and macrophage activity.
- Analysis of intestinal barrier function by measuring barrier proteins and lipopolysaccharide (LPS) levels.
- In vitro assessment of CCFM639's effect on human umbilical vein endothelial cells (HUVECs) for proliferation, motility, and angiogenesis.
- Detection of endothelial nitric oxide synthase (eNOS) expression and investigation of its role using an eNOS inhibitor.
Main Results:
- CCFM639 significantly reduced splenomegaly, pro-inflammatory cytokine levels, and macrophage-driven inflammation in the aorta and coronary arteries.
- The probiotic treatment enhanced intestinal barrier function and improved endothelial cell proliferation, migration, and tube formation.
- CCFM639 administration led to increased eNOS expression, contributing to the alleviation of coronary arteritis in KD mice.
Conclusions:
- Lactobacillus plantarum CCFM639 demonstrates significant anti-inflammatory effects in a Kawasaki disease mouse model.
- CCFM639 shows promise in restoring intestinal barrier function and improving endothelial health.
- This probiotic emerges as a potential therapeutic agent for managing pediatric vasculitis associated with Kawasaki disease.
Abstract:
Kawasaki disease (KD) is an acute inflammatory condition of the blood vessels that primarily manifests in children under five years of age, often leading to coronary artery complications. And KD is the primary contributor to non-congenital cardiac conditions in the pediatric population. In a KD mouse model, Lactobacillus plantarum CCFM639 (CCFM639) was administered, and its effects on systemic and vascular inflammation were evaluated by measuring the spleen index, inflammatory factors, and histopathological changes. Additionally, the effect of CCFM639 on intestinal barrier function was assessed by analyzing barrier protein and serum lipopolysaccharide (LPS) levels. At the cellular level, we evaluated the impact of CCFM639-conditioned medium on endothelial function, including proliferative capacity (CCK-8 assay), directional motility (scratch assay), and tube formation capability (Matrigel angiogenesis assay) in human umbilical vein endothelial cells (HUVECs). The expression levels of endothelial nitric oxide synthase (eNOS) were detected with Western blotting in KD mice, and an eNOS inhibitor was applied to explore role of CCFM639 in alleviating coronary artery inflammation. The results showed that CCFM639 reduced splenomegaly, pro-inflammatory cytokines levels, and macrophage-driven inflammation in the coronary arteries and aorta; enhanced intestinal barrier function; improved endothelial function; and enhanced eNOS expression, thereby alleviating coronary arteritis in KD mice. CCFM639 has emerged as a promising agent for attenuating the pathological inflammatory in pediatric vasculitis syndromes associated with KD.
