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重组人干扰素α-2b反应促进阴道上皮细胞抵御…… (原文此处不完整)

Recombinant Human IFNα-2b Response Promotes Vaginal Epithelial Cells Defense against .

作者信息

Li Ting, Niu Xiaoxi, Zhang Xu, Wang Suxia, Liu Zhaohui

机构信息

Department of Obstetrics and Gynecology, Peking University First HospitalBeijing, China.

Laboratory of Electron Microscopy, Ultrastructural Pathology Center, Peking University First HospitalBeijing, China.

出版信息

Front Microbiol. 2017 Apr 20;8:697. doi: 10.3389/fmicb.2017.00697. eCollection 2017.

Abstract

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 . 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 ( < 0.05). Our scanning electron microscopy results revealed that 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 . Collectively, these responses restored the immune function of the infected VECs against , providing a theoretical basis for this novel treatment strategy.

摘要

由于药物毒性、耐药性、生物利用度和有害的药物相互作用,传统抗真菌药物受到了限制。I型干扰素(IFN)具有直接独特的免疫刺激或免疫调节作用;然而,关于I型干扰素反应诱导的阴道上皮细胞(VECs)的抗真菌反应知之甚少。因此,在本研究中,我们评估了重组人IFNα-2b(rhIFNα-2b)处理后VK2/E6E7 VEC细胞系的细胞毒性活性、免疫活性细胞因子反应和非B IgG产生情况。用rhIFNα-2b处理时,与感染的对照细胞相比,IL-2、IL-4和IL-17的产生显著上调(<0.05)。我们的扫描电子显微镜结果显示, 可通过诱导内吞作用和主动穿透侵入VECs。RhIFNα-2b能够将VECs转变为菌体和伸展模式,促进丝状伪足融合形成片状伪足,并增强VECs的迁移能力和修复能力。此外,rhIFNα-2b可有效抑制 的黏附、菌丝形成和增殖。总的来说,这些反应恢复了受感染VECs对 的免疫功能,为这种新的治疗策略提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ab/5397410/c46071f2e517/fmicb-08-00697-g001.jpg

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