Abstract

BackgroundThe incidence rate of invasive candidiasis is high, its treatment is difficult, and the prognosis is poor. In this study, an immunosuppressive mouse model of invasive Candida albicans (C. albicans) infection was constructed to observe the effects of cinnamaldehyde (CA) on the C. albicans cell wall structure and cell wall (1,3)-β-D-glucan contents. This study provides a theoretical basis for CA treatment to target invasive C. albicans infection.MethodsImmunosuppressed mice with invasive C. albicans infection were given an oral dosage of CA (240 mg.kg− 1.d− 1) for 14 days. Then, mouse lung tissue samples were collected for detection of the levels of (1,3)-β-D-glucan and transmission electron microscopy observations, using fluconazole as a positive control and 2% Tween 80 saline as a negative control.ResultsThe immunosuppressive mouse model of invasive C. albicans infection was successfully established. The levels of (1,3)-β-D-glucan in the CA treatment group, fluconazole positive control group, invasive C. albicans infection immunosuppressive mouse model group, and 2% Tween 80 normal saline control group were 86.55 ± 126.73 pg/ml, 1985.13 ± 203.56 pg/ml, 5930.57 ± 398.67 pg/ml and 83.36 ± 26.35 pg/ml, respectively. Statistically, the CA treatment group, fluconazole positive control group and invasive C. albicans infection immunosuppressive mouse model group were compared with each other (P < 0.01) and compared with the 2% Tween 80 saline group (P < 0.01), showing that the differences were very significant. Comparison of the CA treatment group with the fluconazole positive control group (P < 0.05) displayed a difference as well. Electron microscopy showed that CA destroyed the cell wall of C. albicans, where the outer layer of the cell wall fell off and became thinner and the nuclei and organelles dissolved, but the cell membrane remained clear and intact.ConclusionCA destroys the cell wall structure of C. albicans by interfering with the synthesis of (1,3)-β-D-glucan to kill C. albicans. However, CA does not affect the cell membrane. This study provides a theoretical basis for CA treatment to target invasive C. albicans infection.

Highlights

  • The incidence rate of invasive candidiasis is high, its treatment is difficult, and the prognosis is poor

  • Invasive candidiasis is an infection caused by a yeast, which is a type of fungus, called Candida

  • Construction of an animal model of C. albicans infection in immunosuppressive mice Fungal inspection This program builds animal models based on literature [19, 20]

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Summary

Introduction

The incidence rate of invasive candidiasis is high, its treatment is difficult, and the prognosis is poor. Candida blood infection ( called candidaemia) is the most common form of invasive candidiasis. In the United States, candidaemia is one of the most common causes of blood infections in hospitalized patients [3, 4], which usually leads to long hospital stays and death. It causes high medical expenses [5]. Based on our previous research, CA has good efficacy and safety for the treatment of C. albicans infection in mice [17], and this study further explores the mechanism underlying the effects of CA on Candida in vivo.

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