Transcriptional response of Candida albicans biofilms following exposure to 2-amino-nonyl-6-methoxyl-tetralin muriate

Abstract

Aim: To identify changes in the gene expression profile of Candida albicans (C albicans) biofilms following exposed to 2-amino-nonyl-6-methoxyl-tetralin muriate(10b) and clarify the mechanism of 10b against C albicans biofilms. Methods: Anti-biofilm activity of 10b was assessed by tetrazolium (XTT) reduction assay and the action mechanism against biofilms was investigated by cDNA microarray analysis and real-time RT-PCR assay. Results: Ten differentially expressed genes were directly linked to biofilm formation and filamentous or hyphal growth (eg, NRG1, ECE1 and CSA1). Decreased gene expression was involved in glycolysis (eg, HXK2 and PFK1) and antioxidant defense (eg, SOD5), while increased gene expression was associated with enzymes that specifically hydrolyzed β-1,3 glucan (XOG1), and with lipid, fatty acid and sterol metabolism (eg, SLD1, ERG6 and ERG2). Functional analysis indicated that addition of anti-oxidant ascorbic acid reduced inhibitory efficiency of 10b on mature biofilm. Conclusion: Inhibition of 10b on biofilm formation possibly depends on impairing the ability of C albicans to change its morphology via altering the expression of biofilm formation genes. Mitochondrial aerobic respiration shift and endogenous ROS augmentation might be a major contribution to reduce mature biofilm metabolic activity. The data may be useful for the development of new strategies to reduce the incidence of device-associated infections.

Reactive Oxygen Species-Inducing Antifungal Agents and Their Activity Against Fungal Biofilms

“…Biofilm formation was completely blocked by this compound due to the interference with the yeast-to-hypha transition, the upregulation of an exo-1-3-b-glucanase likely leading to decreased levels of 1-3-b-glucan in the cell wall and biofilm matrix, and other specific targets involved in biofilm formation. Furthermore this compound is active against mature biofilms of C. albicans, and ROS accumulation seems to be correlated with its antibiofilm activity based on a reduced activity measured by the XTT assay in presence of ascorbic acid [106]. Another class of molecules that are able to inhibit biofilm formation of C. albicans and Candida dubliniensis are the marine polyunsaturated fatty acids, such as stearidonic acid (C18:4 n-3), eicosapentaenoic acid (C20:5 n-3) and docosapentaenoic acid [107,108].…”

ROS-dependent anticandidal activity of zinc oxide nanoparticles synthesized by using egg albumen as a biotemplate

“…Unfortunately, most of these drugs, being chemical in nature and having bulk form, are too reactive and unsuitable for human use [3]. With the rising toxicity and development of MDR in C. albicans isolates, the search for new medical treatments beyond conventional antifungal drugs has become a key aim of public health research [4,5]. The failure of drugs to control infection Content from this work may be used under the terms of the Creative Commons Attribution 3.0 licence.…”

Investigating Common Pathogenic Mechanisms between Homo sapiens and Different Strains of Candida albicans for Drug Design: Systems Biology Approach via Two-Sided NGS Data Identification

“…Finally, some of C. albicans SC5314 can go into the host cell by the induced endocytosis, and the others of C. albicans SC5314 form colony morphology by orf19.1059 binding to IL15RA. After receiving signal, orf19.1059 (HHF1) can trigger TFs orf19.1623 (CAP1) and orf19.5908 (TEC1) via signaling proteins orf19.3954 (PSD2), which is affected by orf19.1631 (ERG6)-induced methylation, orf19.1631 (ERG6), which is affected by orf19.3964 (ASH2)-induced methylation, orf19.6082, which is influenced by orf19.169 (CHO2)-induced methylation, orf19.3964 (ASH2), which is influenced by orf19.1631-induced methylation and orf19.705-induced acetylation, orf19.705 (GCN5), orf19.5034 (YBP1), orf19.2616 (UGT51C1), orf19.2306, orf19.4392 (DEM1), orf19.1854 (HHF22), orf19.666, orf19.3760 (DLH1), orf19.2119 (NDT80) and orf19.454 (SFL1) [ 24 , 25 ]. In addition, orf19.2087 (SAS2), which is affected by orf19.705-induced acetylation, triggers TF orf19.1623 (CAP1) indirectly and binds to orf19.939 (NAM7) interacting with orf19.1093 (FLO8).…”