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A Model of Left Ventricular Dysfunction Complicated by CAWS Arteritis in DBA/2 Mice
Naoto Hirata1, Ken-Ichi Ishibashi, Tatsuya Usui
1Department of Pharmacy, Nagano Red Cross Hospital, 5-22-1 Wakasato, Nagano, Nagano 380-8582, Japan.
Abstract:
It was reported previously that a Candida albicans water-soluble fraction (CAWS), including a mannoprotein and β-glucan complex, has strong potency in inducing fatal necrotizing arteritis in DBA/2 mice. In this study, histopathological changes and cardiac function were investigated in this system. One mg/day of CAWS was given to DBA/2 mice via peritoneal injection for five days. The CAWS-treated DBA/2 mice were induced aortitis and died at an incidence of 100% within several weeks. Histological findings included stenosis in the left ventricular outflow tract (LVOT) and severe inflammatory changes of the aortic valve with fibrinoid necrosis. Cardiomegaly was observed and heart weight increased 1.62 fold (P < 0.01). Echocardiography revealed a severe reduction in contractility and dilatation of the cavity in the left ventricle (LV): LV fractional shortening (LVFS) decreased from 71% to 38% (P < 0.01), and the LV end-diastolic diameter (LVDd) increased from 2.21 mm to 3.26 mm (P < 0.01). The titer of BNP mRNA increased in the CAWS-treated group. Severe inflammatory changes resulting from CAWS brought about lethal LV dysfunction by aortic valve deformation with LVOT stenosis. This system is proposed as an easy and useful experimental model of heart failure because CAWS arteritis can be induced by CAWS injection alone.
Insights
Candida albicans water-soluble fraction (CAWS) induces fatal aortitis and heart failure in mice. This study details the histopathological and cardiac changes, proposing a new heart failure model.
Area of Science:
- Immunology
- Cardiology
- Pathology
Background:
- Candida albicans water-soluble fraction (CAWS), a complex of mannoprotein and β-glucan, is known to induce necrotizing arteritis in DBA/2 mice.
- Previous reports indicate CAWS's potent ability to cause severe vascular inflammation.
Purpose of the Study:
- To investigate the histopathological changes and cardiac function in DBA/2 mice following CAWS administration.
- To characterize the induced aortitis and its impact on the heart.
Main Methods:
- DBA/2 mice were administered 1 mg/day of CAWS via peritoneal injection for five consecutive days.
- Histopathological examination of the aorta and heart was performed.
- Echocardiography was used to assess cardiac function, including left ventricular (LV) contractility and dimensions.
- BNP mRNA levels were measured.
Main Results:
- CAWS treatment led to 100% mortality from aortitis within weeks.
- Histology revealed left ventricular outflow tract (LVOT) stenosis, aortic valve inflammation, and fibrinoid necrosis.
- Significant cardiomegaly was observed, with heart weight increasing 1.62-fold (P < 0.01).
- Echocardiography showed reduced LV contractility (LVFS decreased from 71% to 38%, P < 0.01) and LV dilatation (LVDd increased from 2.21 mm to 3.26 mm, P < 0.01).
- BNP mRNA titers were elevated in the CAWS-treated group.
Conclusions:
- CAWS-induced severe inflammation causes lethal left ventricular (LV) dysfunction through aortic valve deformation and LVOT stenosis.
- This experimental system provides a straightforward and effective model for studying heart failure induced by CAWS arteritis.
