Different Host Immunological Response to C. albicans by Human Oral and Vaginal Epithelial Cells
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The immunological mechanisms behind different mucosa against candidiasis are largely unknown. In this study, we investigate the natural protective mechanisms and local cytokine responses of C. albicans-infected oral and vaginal epithelial cells.
The cell lines (Leuk-1 and VK2/E6E7) were cultured with C. albicans (SC5314, Δals3, and Δssa1) in indicated ratio, respectively. The morphological changes and colony growth of C. albicans were observed to evaluate the fungicidal ability of epithelial cells, and the cellular morphological changes and LDH activity measurements were used to assess cell damage. Further, we assess the production of cytokines and chemokines in co-culture supernatants using enzyme-linked immunosorbent assay (ELISA).
Our results show that the oral and vaginal epithelial cells use different strategies to combat this pathogen. Infected oral epithelial cells are adept at the production of cytokines (GM-CSF, IL-1α, and IL-1β) and chemokines (IL-8, MIP-3α, and RANTES), and yet, vaginal cells are more proficient at direct fungal killing. However, both epithelial cells play only a minor role in adaptive immunity to C. albicans. Further, C. albicans Als3p and Ssa1p genes also participate in local immune response since deletion of ALS3 or SSA1 causes reduction in cytokine and chemokine levels in both oral and vaginal cells. The dramatic decreases in both fungal % of cytotoxicity and the secretion of such cytokines as GM-CSF, MIP-3α, and RANTES in Δssa1-infected oral cells were consistent with a delayed germination process in that mutant.
Human oral and vaginal epithelial cells performed different host response to C. albicans by fungal killing ability or secreting cytokines and chemokines.
KeywordsCandida albicans Cytokines Oral epithelial cells Vaginal epithelial cells
This work was supported by National Key Basic Research Program of China (2013CB531605), National Natural Science Foundation of China (No. 81071332), and Jiangsu Provincial Special Program of Medical Science (BL2012003). We thank Professor Li Mao for providing Leuk-1 cell line, Dr. Raina Fichorova for kindly providing cell lines VK2/E6E7, and Dr. Scott G Filler for kindly gift of mutant strains shown in this study. We also would like to thank Professor Wantao Chen for his kind help to our experiment.
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