The Effect of Candida albicans on the Expression Levels of Toll-like Receptor 2 and Interleukin-8 in HaCaT Cells Under High- and Low-glucose Conditions.

The diabetics are prone to skin infections, especially with Candida albicans. It is important to elucidate the different antifungal abilities of patients with hyperglycemia and healthy controls for the treatment of this condition. The toll-like receptor 2 (TLR2) and interleukin (IL)-8 secreted by keratinocytes counteract C. albicans. This study aims to explore the differential expression of toll-like receptor 2 (TLR2) and interleukin (IL)-8 secretion by keratinocytes between controls and diabetic patients when challenged with C. albicans. HaCaT cells were cultured in high-glucose (HG) Dulbecco's modified Eagle's medium (DMEM) and low-glucose (LG) DMEM. Then, they were exposed to C. albicans hyphae for 24 h. The expression levels of TLR2 and IL-8 were determined at different periods in both the HG and LG groups. Real-time polymerase chain reaction analysis, western blotting, and enzyme-linked immunosorbent assays were performed in this study. The morphological changes of HaCaT cells under two different glucose concentrations were also observed. We found that the expression levels of both TLR2 and IL-8 increased and then decreased in the two groups. Notably, the IL-8 levels in the LG group were higher than those in the HG group at each time point (P <0.05), and the TLR2 levels in the LG group were higher than those in the HG group at the beginning of the experiment and after 24 h of treatment with C. albicans (P <0.05). In each group, the levels of IL-8 and TLR2 at the secretion peak were significantly different from those in the initial and the last period of observation (P <0.05). The cellular morphology of HaCaT cells treated with different concentrations of glucose was also similar. However, with prolonged coculture time, cell death increased. These observations showed that TLR2 and IL-8 act on the keratinocytes interacting with C. albicans, and HG status might affect the function of HaCaT cells by reducing the secretion of IL-8 and TLR2.