The putative ABC transporter encoded by the orf19.4531 plays a role in the sensitivity of Candida albicans cells to azole antifungal drugs.

ATP-binding cassette (ABC) transporters constitute a large superfamily of integral membrane proteins in prokaryotic and eukaryotic cells. In the human fungal pathogen Candida albicans, there are 28 genes encoding ABC transporters and many of them have not been characterized so far. The orf19.

Berberine inhibits fluphenazine-induced up-regulation of CDR1 in Candida albicans.

Over-expression of the Candida drug resistance gene CDR1 is a common mechanism generating azole-resistant Candida albicans in clinical isolates. CDR1 is transcriptionally activated through the binding of the transcription factor Tac1p to the cis-acting drug-responsive element (DRE) in its promoter. We previously demonstrated that the combination of fluconazole (FLC) and berberine (BBR) produced significant synergy when used against FLC-resistant C.

Transposition of the Zorro2 retrotransposon is activated by miconazole in Candida albicans.

Zorro2 is a member of a non-long terminal repeat (LTR) retrotransposon family in Candida albicans, but as yet no clear evidence has been provided to establish either transcription or transposition activity for Zorro2. In this study, the relative expression changes of two open reading frames in Zorro2, ORF19.7274 and ORF19.

S100A10 downregulation inhibits the phagocytosis of Cryptococcus neoformans by murine brain microvascular endothelial cells.

Cryptococcus neoformans invades the central nerve system through endocytosis by the vascular endothelia. S100A10 interacts with Ca(2+) channel proteins in the vascular endothelia and regulates the filamentous actin network. We hypothesized that S100A10 was involved in the pathogenesis of cryptococcosis and sought to investigate here the effect on the phagocytosis and growth of C.

High-frequency genetic contents variations in clinical Candida albicans isolates.

Genome plasticity is a hallmark of Candida albicans and is believed to be an adaptation strategy. But the extent of such genomic variability is not well investigated. In this study, genetic contents of clinical C.

[Advances in the study of Candida albicans gene mutation on azole drug resistance].

Gene mutation of Candida albicans is one of the main causes for azole drug resistance. Different types of variation play different roles in promoting the process of drug resistance. ERG series of gene mutations primarily affect the ergosterol synthesis pathway.

A novel polyamide SL-A92 as a potential fungal resistance blocker: synthesis and bioactivities in Candida albicans.

Aim: To synthesize a novel polyamide SL-A92 and evaluate its bioactivity against drug resistance in Candida albicans.

Methods: SL-A92 was synthesized using N-hydroxybenzotriazole (HOBT)/N,N'-dicyclohexylcarbodiimide (DCC) in solution phase. Its antifungal activities and effects on strain growth were tested using the micro-broth dilution method and growth curves, respectively.

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

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).

TOP2 gene disruption reduces drug susceptibility by increasing intracellular ergosterol biosynthesis in Candida albicans.

In this study the role of the TOP2 gene in fungal drug susceptibility was investigated by disrupting and overexpressing the gene in Candida albicans. MIC determination and a spot assay showed that a top2Delta/Delta null mutant (strain T2bc) was more resistant to the antifungals tested than the wild-type (strain CAI4). Real-time RT-PCR and rhodamine 6G efflux examination showed that TOP2 did not influence the activity of drug efflux pumps.

2-Amino-nonyl-6-methoxyl-tetralin muriate inhibits sterol C-14 reductase in the ergosterol biosynthetic pathway.

Aim: To investigate the action mechanism of a novel chemical structural aminotetralin derivate, 2-Amino-Nonyl-6-Methoxyl-Tetralin Muriate (10b), against Candida albicans (C albicans) in the ergosterol biosynthetic pathway.

Methods: Antifungal susceptibility test of 10b was carried out using broth microdilution method, the action mechanism of 10b against C albicans was investigated by GC-MS spectrometry and real-time RT-PCR assay, and cytotoxicity of 10b in vitro was assessed by MTS/PMS reduction assay.

Results: 10b reduced the ergosterol content markedly, and the 50% ergosterol content inhibitory concentration (ECIC(50) value) was 0.

Proteomic analysis reveals a synergistic mechanism of fluconazole and berberine against fluconazole-resistant Candida albicans: endogenous ROS augmentation.

Our previous study showed that concomitant use of berberine (BBR) and fluconazole (FLC) provided a synergistic action against FLC-resistant Candida albicans (C. albicans) clinical strains in vitro. To clarify the mechanism underlying this action, we performed a comparative proteomic study in untreated control cells and cells treated with FLC and/or BBR in 2 clinical strains of C.

Baicalein induces programmed cell death in Candida albicans.

Recent evidence has revealed the occurrence of an apoptotic phenotype in Candida albicans that is inducible with environmental stresses such as acetic acid, hydrogen peroxide, and amphotericin B. In the present study, we found that the Chinese herbal medicine Baicalein (BE), which was one of the skullcapflavones, can induce apoptosis in C. albicans.

The alternative oxidase of Candida albicans causes reduced fluconazole susceptibility.

Objectives: To evaluate the effect of Candida albicans mitochondrial respiratory status on antifungal azole susceptibility.

Methods: The inhibitors cyanide and salicylhydroxamic acid (SHAM) were each combined with azoles to examine the effect of the combinations on C. albicans.

Ascorbic acid decreases the antifungal effect of fluconazole in the treatment of candidiasis.

1. The aim of the present study was to investigate the effects of ascorbic acid (AA) on the antifungal activity of fluconazole (FCZ) in a systemic murine candidiasis model as well as in vitro. 2.

[Advances in the chemical and biological studies of polyamides].

Polyamides, containing N-methylpyrrole (Py) and N-methyl-imidazole (Im) amino acids, are synthetic oligomers programmed to read the DNA double helix in the minor groove with high affinities and sequence specificities resulting in modulation of gene expression. They are cell permeable, stable and have no cytotoxicity, which provide a promising tool of gene regulation. We describe here recent advances in the field of DNA binding polyamides, including pairing rules, specifities and affinities to DNA, synthesis methods, cellular and nuclear uptake properties, gene regulation and effectiveness in vivo.

DNA microarray analysis of fluconazole resistance in a laboratory Candida albicans strain.

Several mechanisms are responsible for the acquired fluconazole (FLC) resistance in Candida albicans. In this study, we developed a FLC-resistant C. albicans strain through serial cultures of a FLC-susceptible C.

Candida albicans cells lacking CaMCA1-encoded metacaspase show resistance to oxidative stress-induced death and change in energy metabolism.

Candida albicans, an opportunistic pathogen, can undergo programmed cell death upon various stimuli, including oxidative stress. In this study, we showed that deletion of CaMCA1, a homologue of Saccharomyces cerevisiae metacaspase YCA1, could both attenuated oxidative stress-induced cell death and caspase activation. Compared to wild-type strain, Camca1Delta mutant showed higher accumulation of trehalose and transcription of the genes related to trehalose biosynthesis (TPS2 and TPS3) under the condition of oxidative stress.

RTA2, a novel gene involved in azole resistance in Candida albicans.

Widespread and repeated use of azoles, particularly fluconazole, has led to the rapid development of azole resistance in Candida albicans. Overexpression of CDR1, CDR2, and CaMDR1 has been reported contributing to azole resistance in C. albicans.

In vitro activity of baicalein against Candida albicans biofilms.

Candidiasis can be associated with the formation of biofilms on bioprosthetic surfaces. The intrinsic resistance of Candida albicans biofilms to the most commonly used antifungal agents has been demonstrated. Here we examined the effect of baicalein (BE) on C.

Changtai granule, a traditional Chinese drug, protects hapten-induced colitis by attenuating inflammatory and immune dysfunctions.

The study was aimed to investigate the effects and mechanism of action of Changtai granule (CT), a traditional compound Chinese medicinal formula, in rodent 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis. Rats with TNBS/ethanol-induced colitis were used. The colonic wet weight, myeloperoxidase (MPO) activity, macroscopic and histological colon injury was observed.

CaIPF7817 is involved in the regulation of redox homeostasis in Candida albicans.

CaIPF7817, a functionally unknown gene in Candida albicans, was suggested to be involved in the redox system previously, but its exact role is unknown. In this study, ipf7817 null mutant was generated with the URA-blaster method. After the deletion of CaIPF7817, intracellular levels of reactive oxygen species were significantly increased; mitochondrial membrane potential, a direct indicator of mitochondrial function, was elevated; some important redox-related genes, including GLR1, SOD2, and TRR1, were up-regulated; and the GSH/GSSG ratio was raised.

Proteomic analysis reveals a metabolism shift in a laboratory fluconazole-resistant Candida albicans strain.

Multifactorial and multistep alterations are involved in acquired fluconazole (FLC) resistance in Candida albicans. In this study, a FLC-resistant C. albicans strain was obtained by serial cultures of a FLC-susceptible C.

Fcr1p inhibits development of fluconazole resistance in Candida albicans by abolishing CDR1 induction.

Overexpression of Candida drug resistance 1 (CDR1) gene in Candida albicans (C. albicans), an efflux pump, is one of the major mechanisms contributing to drug resistance. C.

In vitro and in vivo activities of HQQ-3, a new triazole antifungal agent.

The activity of HQQ-3, a new triazole antifungal agent, was evaluated and compared with those of fluconazole, ketoconazole and terbinafine in vitro and with fluconazole in vivo. HQQ-3 exhibited potent in vitro activity against clinically important fungi. The activity of HQQ-3 against Candida spp.

Lymphtoxin beta receptor-Ig protects from T-cell-mediated liver injury in mice through blocking LIGHT/HVEM signaling.

LIGHT is a member of the TNF superfamily, which is transiently expressed on the surface of activated T lymphocytes and immature dendritic cells. Its known receptors are herpesvirus entry mediator (HVEM) prominently in T lymphocytes, and lymphtoxin beta receptor (LTbetaR) in stromal cells or nonlymphoid hematopoietic cells. Previous studies have shown that overexpression of LIGHT on T cells could lead to autoimmune reaction including lymphocytes activation, inflammation, and tissue destruction.