Lactobacillus plantarum CCFM639 ameliorates vascular dysfunction in mice with Kawasaki disease involving eNOS/NO pathway.

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.