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Fungal-Host Interaction: Curcumin Modulates Proteolytic Enzyme Activity of Candida albicans and Inflammatory Host Response In Vitro

机译:真菌-宿主相互作用:姜黄素调节白色念珠菌和体外炎症性宿主反应的蛋白水解酶活性。

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摘要

Current treatments for Candida albicans infection are limited due to the limited number of antifungal drugs available and the increase in antifungal resistance. Curcumin is used as a spice, food preservative, flavoring, and coloring agent that has been shown to have many pharmacological activities. Thus, this study evaluated the modulatory effects of curcumin on major virulence factors associated with the pathogenicity of C. albicans. The minimum inhibitory concentration (MIC) of curcumin against C. albicans (SC5314) was determined. Biofilm formation was quantified and the proteinase and phospholipase secretion was measured. The cytotoxicity was tested in oral fibroblast cells. A cocultured model was used to analyze the gene expression of proinflammatory cytokines (IL-1β, IL-1α, and IL-6) from host cells, as well SAP-1 and PLB-1 by RT-PCR. The MIC was between 6.25 and 12.5 µM, and the activity of proteinase enzyme was significantly decreased in biofilms treated with curcumin. However, proteinase gene expression was not downregulated after curcumin treatment. Furthermore, gene expressions of host inflammatory response, IL-1β and IL-1α, were significantly downregulated after exposure to curcumin. In conclusion, curcumin exhibited antifungal activity against C. albicans and modulated the proteolytic enzyme activities without downregulating the gene expression. In host inflammatory response, curcumin downregulated IL-1β and IL-1α gene expression.
机译:由于可用的抗真菌药物数量有限以及抗真菌抗药性增加,目前用于白色念珠菌感染的治疗受到限制。姜黄素用作香料,食品防腐剂,调味剂和着色剂,已显示具有许多药理活性。因此,本研究评估了姜黄素对与白色念珠菌致病性相关的主要毒力因子的调节作用。确定姜黄素对白色念珠菌(SC5314)的最小抑制浓度(MIC)。定量生物膜的形成并测量蛋白酶和磷脂酶的分泌。在口服成纤维细胞中测试了细胞毒性。使用共培养模型通过RT-PCR分析来自宿主细胞的促炎细胞因子(IL-1β,IL-1α和IL-6)以及SAP-1和PLB-1的基因表达。 MIC在6.25至12.5µM之间,用姜黄素处理的生物膜中蛋白酶的活性显着降低。然而,姜黄素处理后蛋白酶基因表达并未下调。此外,暴露于姜黄素后,宿主炎症反应的基因表达IL-1β和IL-1α显着下调。总之,姜黄素对白念珠菌具有抗真菌活性,并在不下调基因表达的情况下调节蛋白水解酶的活性。在宿主炎症反应中,姜黄素下调IL-1β和IL-1α基因表达。

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