Background: The cause of Kawasaki disease (KD) has been still unknown though the intestinal flora was reported as one of the candidate etiology of KD. Candida is known as one of the intestinal flora. Intraperitoneal injection of Candida albicans water-soluble fractions (CAWS) that compose of polysaccharide of cell wall of the yeast can induce systemic vasculitis in mice. It is evaluated as animal model of Kawasaki disease vasculitis because this experimental vasculitis is similar to those observed in KD patients. However it is uncertain whether or not oral administration of CAWS can induce vasculitis in mice. Aim: The present study aimed to elucidate whether or not oral administration of CAWS can induce vasculitis. Materials and methods: Mice, DBA/2, male, 4 weeks of age were used. CAWS suspended in PBS was administered perorally to mice for 28 consecutive days. As a priming agent, 20 micrograms of LPS was injected to mice intraperitoneally before administration of CAWS. Experimental groups are as follows. Group-I : Peroral administration of 800 micrograms of CAWS with LPS, Group-II: Peroral administration of 800 micrograms of CAWS without LPS, Group-III : Peroral administration of 250 micrograms of CAWS with LPS. Mice injected CAWS intraperitoneally (conventional procedure) were used as control group. Vasculitis was evaluated by routine histological techniques. This study conformed with regulations of position of the American Heart Association on research animal use and Toho University’s Animal Ethics Committee. Result: The incidence of vasculitis in each group were as follows : Group-I : 1/6, Group-II:0/6, Group-III:1/6, Control : 3/3. Dense infiltration of neutrophils and macrophages was observed in coronary artery and/or aortic root. Severity of inflammatory cell infiltration and extent of the lesion in Group-I and Group-III were milder and smaller than those of control. Conclusion: Present study revealed that peroral administration of CAWS could induce vasculitis in mice though the incidence of vasculitis was lower than that of control. This model is considered to be useful to clarify the relation between intestinal immunity and vasculitis. We should clarify the mechanism that oral administration of CAWS induced vasculitis.
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