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棕榈酸抑制:生物膜、细胞表面疏水性、麦角固醇生物合成及酶活性等毒力因子。

Palmitic Acid Inhibits the Virulence Factors of : Biofilms, Cell Surface Hydrophobicity, Ergosterol Biosynthesis, and Enzymatic Activity.

作者信息

Prasath Krishnan Ganesh, Tharani Hariharan, Kumar Mourya Suraj, Pandian Shunmugiah Karutha

机构信息

Department of Biotechnology, Alagappa University, Karaikudi, India.

出版信息

Front Microbiol. 2020 May 8;11:864. doi: 10.3389/fmicb.2020.00864. eCollection 2020.

Abstract

Biofilm is the fortitude of species infections which eventually causes candidiasis in human. is one of the predominant species commonly found in systemic infections, next to . In species, biofilm maturity initiates irreversible surface attachment of cells and barricades the penetration of conventional antifungals. Hence, the current study investigated the antifungal and antivirulence potency of palmitic acid (PA) against mature biofilm and its associated virulence factors. results revealed an effective inhibition of biofilm in PA-treated , compared to and . Also, PA reduced mature biofilm at various time points. Further, PA treatment triggered apoptosis in through ROS mediated mitochondrial dysfunction as demonstrated by confocal microscopic observation of PI, DAPI and DCFDA staining. PA regulated other virulence factors such as cell surface hydrophobicity, ergosterol biosynthesis, protease and lipase after 48 h of treatment. Downregulation of (Lanosterol 14-alpha demethylase) was contributed to the reduction of ergosterol in PA-treated . However, enhanced hyphal growth was observed in PA-treated through upregulation (Hyphal wall protein) and (Enhanced filamentous growth). This study highlighted the antibiofilm and antivirulence potency of PA against . Hence, PA could be applied synergistically with other antifungal agents to increase the efficacy for regulating NCAC infections.

摘要

生物膜是导致人类念珠菌病的物种感染的坚固防线。是系统性感染中常见的主要物种之一,仅次于。在物种中,生物膜成熟会引发细胞不可逆地附着于表面,并阻碍传统抗真菌药物的渗透。因此,本研究调查了棕榈酸(PA)对成熟生物膜及其相关毒力因子的抗真菌和抗毒力效力。结果显示,与和相比,PA处理的中生物膜受到有效抑制。此外,PA在不同时间点减少了成熟生物膜。进一步的研究表明,通过共聚焦显微镜观察PI、DAPI和DCFDA染色发现,PA处理通过ROS介导的线粒体功能障碍引发了细胞凋亡。PA在处理48小时后调节了其他毒力因子,如细胞表面疏水性、麦角固醇生物合成、蛋白酶和脂肪酶。(羊毛甾醇14-α脱甲基酶)的下调导致PA处理的中麦角固醇减少。然而,通过上调(菌丝壁蛋白)和(增强丝状生长),在PA处理的中观察到菌丝生长增强。本研究强调了PA对的抗生物膜和抗毒力效力。因此,PA可与其他抗真菌药物协同应用,以提高调节NCAC感染的疗效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c0e/7226919/6a262f0cb94c/fmicb-11-00864-g001.jpg

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