Th1 immunity induction by ginsenoside Re involves in protection of mice against disseminated candidiasis due to Candida albicans.

Type-1 and -2 responses of T helper lymphocytes demonstrate essentially different and opposite effector functions. In the present study, we determined the immunoregulatory effect of ginsenoside Re against disseminated candidiasis due to Candida albicans. This fungus may be one of the most problematic fungi for humans. Results showed that Re had no growth-inhibitory effect on C. albicans. In contrast, mice groups given Re intraperitoneally before intravenous challenge with live C. albicans survived longer against disseminated candidiasis than Re-untreated mice. All of the ten control mice died by day 15, whereas seven out of ten Re-treated mice survived during the entire duration of the 40 day-observation resulting in mean survival times (MST) of 32.7 ± 13.4 (MST ± S.E.) days. These survival values were almost the same as the values obtained from Rg1-treated mice used for a positive control. Through determining the kidneys' candidal colony forming unit, we found that the disease severity of Re-treated mice was far less than that of Re-untreated animals. This protection was transferable by the CD4+T cells (RECD4T) from Re-treated mice similar to (RGCD4T) CD4+T cells from Rg1-treated animals. A cytokine profile revealed the Th1- lineage development of dominant IFNg and IL-2 from RECD4T. However, the protection was abolished when mice were treated with anti-mouse IFNg. In addition, a hemolytic assay showed that Re at 1000 μg/ml caused no hemolysis. All of these data indicate that Re has the immunoregulatory effect of CD4+T cell-mediated immune response that is led from a Type 1-dominant immunity.