Microorganism infection has been reported to associate with many cancers. We adopt a carcinogen-induced mouse oral cancer model to investigate the effect of oral Candida albicans infection on the development of oral cancer. We observed that exposure of Candida increased the incidence of oral cancer. The expression of genes involved in the Th17 development pathway was elevated in the tumor microenvironment. A co-localization of Candida mycelium and presence of IL-1beta, IL-6, IL-17A, IL-17F, and IL-22 was demonstrated. Exposure of mouse oral epithelial cells to curdlan, a component of Candida cell wall, triggered the release of MCP-1 which can recruit monocyte and macrophage. Exposure of mouse monocyte to curdlan in turn modulated the differentiation of macrophages and dendritic cells and promoted the production of arginase, iNOS, IL-1beta, IL-6 ad IL-23. In addition, curdlan promoted the differentiation of myeloid-derived suppressor cells. These conditions may further promote the development of Th17 cells. We demonstrated that Candida albicans infection creates a microenvironment favoring MDSC and Th17 development and promotes mouse oral cancer incidence.
