Recombinant Human IFNα-2b Response Promotes Vaginal Epithelial Cells Defense against Candida albicans.
Recombinant Human IFNα-2b Response Promotes Vaginal Epithelial Cells Defense against Candida albicans.
复制标题
重组人 IFNa-2b 反应促进阴道上皮细胞防御白色念珠菌
DOI：
10.3389/fmicb.2017.00697
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发表时间：
2017
影响因子：
5.2
通讯作者：
Liu Z
中科院分区：
文献类型：
--
作者：
Li T;Niu X;Zhang X;Wang S;Liu Z
由于药物毒性、耐药性、生物利用度和有害的药物相互作用，经典的抗真菌药物受到限制。I型干扰素（IFN）发挥直接不同的免疫刺激或免疫调节作用，然而，鲜为人知的是关于抗真菌反应的阴道上皮细胞（VEC）诱导的I型IFN反应。因此，在本研究中，我们评估了重组人IFN α-2b（rhIFNα-2b）处理后VK 2/E6 E7 VEC细胞系对白色念珠菌的细胞毒活性、免疫活性细胞因子应答和非B IgG产生。rhIFNα-2b处理后，IL-2、IL-4和IL-17的分泌均显著高于感染对照组（P < 0.05）。扫描电子显微镜结果显示，C.白色念珠菌可以通过诱导内吞和主动渗透侵入VEC。rhIFNα-2b可使VECs向叶状体和伸展型转化，促进丝状伪足融合形成片状伪足，增强VECs的运动性和修复能力。rhIFNα-2b能有效抑制C.白色念珠菌。总的来说，这些反应恢复了受感染的VEC对C.白念珠菌的体外培养，为这种新的治疗策略提供了理论基础。
Classical antifungal drugs have been subjected to restrictions due to drug toxicity, drug resistance, bioavailability, and detrimental drug interactions. Type I interferon (IFN) exerts direct distinct immunostimulatory or immunomodulatory actions; however, little is known regarding the anti-fungal reactions of vaginal epithelial cells (VECs) induced by the type I IFN response. Therefore, in the present study, we evaluated the cytotoxic activity, immunocompetent cytokine responses, and non-B IgG production of the VK2/E6E7 VEC line following recombinant human IFN α-2b (rhIFNα-2b) treatment in response to Candida albicans. When treated with rhIFNα-2b, the production of IL-2, IL-4, and IL-17 were significantly up-regulated compared to the infected control cells (P < 0.05). Our scanning electron microscopy results revealed that C. albicans can invade VECs by inducing both endocytosis and active penetration. RhIFNα-2b was able to transform the VECs into a thallus and stretched pattern, promoting the fusion of filopodia to form a lamellipodium and enhancing the mobility and the repair capacity of the VECs. In addition, rhIFNα-2b could effectively inhibit the adhesion, hyphal formation, and proliferation of C. albicans. Collectively, these responses restored the immune function of the infected VECs against C. albicans in vitro, providing a theoretical basis for this novel treatment strategy.