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首页> 外文期刊>Infection and immunity >Deregulated Production of Protective Cytokines in Response to Candida albicans Infection in Patients with Chronic Mucocutaneous Candidiasis
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Deregulated Production of Protective Cytokines in Response to Candida albicans Infection in Patients with Chronic Mucocutaneous Candidiasis

机译：慢性粘膜皮肤念珠菌病患者对白色念珠菌感染的保护性细胞因子生产失控

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Patients with chronic mucocutaneous candidiasis (CMC) are selectively unable to clear the yeast Candida, which results in persistent debilitating infections affecting the skin, nails, and mucous membranes. The underlying defect is unknown. Recent animal studies highlighted the importance of type 1 cytokines in protection against Candida, and previous work suggested that CMC patients may exhibit altered cytokine production in response to Candida. Based on these findings, in this study we investigated cytokine production in CMC patients by assessing a range of inflammatory, anti-inflammatory, type 1, and type 2 cytokines (interleukin-2 [IL-2], IL-4, IL-5, IL-6, IL-10, IL-12, gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α]) in whole-blood cultures in response to five different fractions of Candida albicans (carbohydrate, purified mannan, and protein-rich fractions, etc.), as well as non-Candida antigens. Our results demonstrate that cytokine production is deregulated in a Candida-specific way for some cytokines (IL-2, IL-10), is deregulated more generally for other cytokines (IL-12, IL-6, IFN-γ), and is not markedly altered for still other cytokines (TNF-α, IL-4, IL-5). The most notable finding in CMC patients was the markedly impaired production of IL-12 in parallel with dramatically increased levels of IL-6 and IL-10 that occurred selectively in response to Candida. These results suggest that patients with CMC have impaired production of type 1-inducing cytokines (possibly a macrophage or dendritic cell defect?), which could result in an inability to mount protective cell-mediated responses and a failure to clear Candida. Continued tissue damage and inflammation may trigger production of high levels of inhibitory cytokines, such as the IL-10 production seen in our study, which would further reduce production of type 1-inducing cytokines in a positive feedback loop leading to persistent infection.
机译：患有慢性粘膜皮肤念珠菌病（CMC）的患者选择性地无法清除酵母菌 Candida ，这会导致持续衰弱的感染影响皮肤，指甲和粘膜。潜在的缺陷是未知的。最近的动物研究强调了1型细胞因子在预防 Candida 方面的重要性，而先前的研究表明CMC患者对 Candida的反应可能会改变细胞因子的产生。 ，在这项研究中，我们通过评估一系列炎症，抗炎，1型和2型细胞因子（白介素2 [IL-2]，IL-4，IL-5，IL-6 ，全血培养物中IL-5，IL-12，γ-干扰素[IFN-γ]，肿瘤坏死因子α[TNF-α]）对五种不同的白色念珠菌（碳水化合物）的响应，纯化的甘露聚糖和富含蛋白质的组分等）以及非 Candida 抗原。我们的结果表明，某些细胞因子（IL-2，IL-10）以 Candida 特异性方式解除了细胞因子的生产，而其他细胞因子（IL-12，IL-6， IFN-γ），并且对于其他细胞因子（TNF-α，IL-4，IL-5）没有明显改变。在CMC患者中最显着的发现是IL-12的生产明显受损，同时对 Candida有选择性地发生的IL-6和IL-10水平显着升高。这些结果表明，这些患者CMC感染的人会削弱1型诱导细胞因子（可能是巨噬细胞或树突状细胞缺陷？）的产生，这可能导致无法进行保护性细胞介导的反应并且无法清除 Candida。组织损伤和炎症可能触发高水平抑制性细胞因子的产生，例如在我们的研究中发现的IL-10产生，这将进一步减少导致持续感染的正反馈回路中1型诱导型细胞因子的产生。

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