Distinct expressions of immunoglobulin signal related molecules between human Kawasaki disease and BALB/c mice treated with Lactobacillus casei cell wall extract

Background: Kawasaki disease (KD) is an acute febrile multi-system vasculitic syndrome occurring mostly in infants and children. It is also the most commonly acquired heart disease in children. The exact etiology and pathogenesis of KD remain unclear. Genome-wide association study identified FCGR2A, CD40 and B lymphoid tyrosine kinase (BLK) to be susceptibility locus for Kawasaki disease. Plasma clusterin level was also noted being able to predict the occurrence of CAL and IVIG resistance of KD. Single intraperitoneal injections of Lactobacillus casei cell wall extract (LCWE) inducing an acute inflammatory coronary arteritis in mice is reported resemble the coronary arteritis found in KD. This study was conducted to investigate whether these immunoglobulin-related significant molecules (clusterin, BLK, CD40/CD40L, and Fcγ receptor that observed in human KD are also play important roles in LCWE treated mice. Material and methods: Wild-type male BALB/c mice were intraperitoneally injected with LCWE (1 mg/mL) to induce vasculitis. The target molecules in mice were examined post injections as indicated. Results: There was higher Fcγ receptor IIIA (CD16) expression on CD4+ splenocytes of LCWE treated mice than control group. However, LCWE treatment did not change the CD40, CD40L and Fγ receptor IIB expression of splenocytes. LCWE treatment also did not change BLK abundance of splenocytes. Plasma clusterin level did not alter after LCWE treatment at day 3, 7 or day 14. Conclusion: There are many inconsistent expressions between LCWE-treated mice and Kawasaki disease in human. Thus LCWE-treated mice cannot totally present human KD. We should be very carefully when apply the laboratory finding of LCWE-treated mice to human KD.