Abstract: AIM: To investigate the immunological mechanisms of allicin in anti-candidiasis, with a view to provide scientific basis for clinical treatment to systemic candidiasis.METHODS: The murine models of systemic candidiasis were established in normal and immuno-suppressional mice, and then the normal and immuno-suppressional mice were separately divided into two groups: control group and treatment group. Each treatment group was given allicin for one course, while control group was given normal saline. At the end of treatment, the effect of allicin in the proliferation activity of spleen T lymphocytes, the level of IFN-γ and the number of viable C.a in organs were detected by MTT, sandwich ELISA and plate colony count respectively.RESULTS: Identified via histopathology, the murine model of systemic candidiasis was established successfully. After treated by allicin for one course, the proliferation activity of spleen T lymphocytes and the level of IFN-γ in treatment group, which compared with control group, were both significantly increased, and had significant differences(P＜0.01). The number of viable C.a in organs in treatment group was lower than that in control group, which also had significant difference(P＜0.01). CONCLUSION: Allicin can enhance the proliferation activity of spleen T lymphocytes and the level of IFN-γ, and reduce the number of viable C.a in organs in both normal and immuno-suppressional mice.

Key words: Candida albicans, Allicin, IFN-γ, Immunity