Antibiofilm and antivirulence activities of 6-gingerol and 6-shogaol against Candida albicans due to hyphal inhibition
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ABSTRACT:
PROVIDER: PRJNA481457 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7529400_1.fastq.gz | Fastqsanger.gz | |||
| SRR7529400_2.fastq.gz | Fastqsanger.gz | |||
| SRR7529401_1.fastq.gz | Fastqsanger.gz | |||
| SRR7529401_2.fastq.gz | Fastqsanger.gz | |||
| SRR7529402_1.fastq.gz | Fastqsanger.gz |
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Project description:Candida albicans is an opportunistic pathogen and responsible for candidiasis. C. albicans readily forms biofilms on various biotic and abiotic surfaces, and these biofilms can cause local and systemic infections. C. albicans biofilms are more resistant than its free yeast to antifungal agents and less affected by host immune responses. Transition of yeast cells to hyphal cells is required for biofilm formation and is believed to be a crucial virulence factor. In this study, six components of ginger were investigated for antibiofilm and antivirulence activities against a fluconazole-resistant C. albicans strain. It was found 6-gingerol, 8-gingerol, and 6-shogaol effectively inhibited biofilm formation. In particular, 6-shogaol at 10 µg/ml significantly reduced C. albicans biofilm formation but had no effect on planktonic cell growth. Also, 6-gingerol and 6-shogaol inhibited hyphal growth in embedded colonies and free-living planktonic cells, and prevented cell aggregation. Furthermore, 6-gingerol and 6-shogaol reduced C. albicans virulence in a nematode infection model without causing toxicity at the tested concentrations. Transcriptomic analysis using RNA-seq and qRT-PCR showed 6-gingerol and 6-shogaol induced several transporters (CDR1, CDR2, and RTA3), but repressed the expressions of several hypha/biofilm related genes (ECE1 and HWP1), which supported observed phenotypic changes. These results highlight the antibiofilm and antivirulence activities of the ginger components, 6-gingerol and 6-shogaol, against a drug resistant C. albicans strain.
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Project description:Biofilms are sessile microbial communities that are often resistant to conventional antimicrobial therapeutics and the host immune system. Candida albicans is an opportunistic pathogenic yeast and responsible for candidiasis. It readily colonizes host tissues and implant devices, and forms biofilms, which play an important role in pathogenesis and drug resistance. Its morphological transition from budding yeast to hyphal form and subsequent biofilm formation is regarded as the crucial factor for drug tolerance and virulence of Candida infections. In this study, nepodin (also called musizin) from Rumex japonicus root was investigated for antibiofilm, antihyphae, and antivirulence activities against fluconazole-resistant C. albicans strain. Nepodin at 2 µg/ml from Rumex plant effectively inhibited C. albicans biofilm formation by more than 90% but had no effect on planktonic cell growth. Also, Rumex root extract and nepodin inhibited hyphal growth and cell aggregation of C. albicans. Interestingly, nepodin also showed antibiofilm activity against Staphylococcus aureus or A. baumannii strains and two systems of dual biofilms of C. albicans and S. aureus or A. baumannii, respectively. Transcriptomic analysis using RNA-seq and qRT-PCR showed nepodin repressed the expressions of several hypha/biofilm related genes (ECE1, HWP1, and UME6) and overexpressed several transport genes (CDR4, CDR11, IFD6, and TPO2), which supported observed phenotypic changes.
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Project description:Candida albicans is an opportunistic pathogen and responsible for candidiasis. C. albicans readily forms biofilms on various biotic and abiotic surfaces, and these biofilms can cause local and systemic infections. C. albicans biofilms are more resistant than its free yeast to antifungal agents and less affected by host immune responses. Transition of yeast cells to hyphal cells is required for biofilm formation and is believed to be a crucial virulence factor. In this study, six components of ginger were investigated for antibiofilm and antivirulence activities against a fluconazole-resistant C. albicans strain. It was found 6-gingerol, 8-gingerol, and 6-shogaol effectively inhibited biofilm formation. In particular, 6-shogaol at 10 ?g/ml significantly reduced C. albicans biofilm formation but had no effect on planktonic cell growth. Also, 6-gingerol and 6-shogaol inhibited hyphal growth in embedded colonies and free-living planktonic cells, and prevented cell aggregation. Furthermore, 6-gingerol and 6-shogaol reduced C. albicans virulence in a nematode infection model without causing toxicity at the tested concentrations. Transcriptomic analysis using RNA-seq and qRT-PCR showed 6-gingerol and 6-shogaol induced several transporters (CDR1, CDR2, and RTA3), but repressed the expressions of several hypha/biofilm related genes (ECE1 and HWP1), which supported observed phenotypic changes. These results highlight the antibiofilm and antivirulence activities of the ginger components, 6-gingerol and 6-shogaol, against a drug resistant C. albicans strain.
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Project description:Deleting components of the Arp2/3 complex in Candida albicans resulted in a global lack of hyphal specific gene induction. This observation suggests that the failure in hyphal growth of Arp2/3 complex mutants could be a result of failure to activate hyphal specific genes. If the hyphal defect was primarily due to failure to activate gene expression, de-repressing hyphal-specific gene expression by deleting the NRG1 repressor could potentially suppress the defect, as deletion of NRG1 leads to constitutive filamentous growth even in the absence of any hyphal induction signals (Garcia-Sanchez et al., 2005, Kadosh & Johnson, 2005). We therefore created an nrg1Î/Îarp2Î/Î mutant. When grown under non-inducing conditions, nrg1Î/Îarp2Î/Î cells showed the arp2Î/Î mutant morphology of round and swollen cells. When induced for hyphal growth, nrg1Î/Îarp2Î/Î cells also exhibited the arp2Î/Î cell morphology and did not form hyphae even after extended overnight incubation times. To determine if the hyphal-specific genes are de-repressed in the nrg1Î/Îarp2Î/Î mutant, we performed transcript profiling. We compared the nrg1Î/Îarp2Î/Î mutant grown under hyphal conditions to the arp2Î/Î mutant grown under the same conditions (10% serum, 37ï°C, three hours), and found that a significant number of hyphal-specific genes that are normally induced when WT cells are undergoing the yeast to hyphae switch (WT-HY) showed greater expression in the nrg1Î/Îarp2Î/Î mutant compared to arp2Î/Î cells (p-value 4.9x10-9). When we examined the set of NRG1-dependent hyphal-specific genes previously identified (Kadosh & Johnson, 2005), we found that seven of 28 genes (HYR1, SAP5, SAP4, KIP4, ORF19.6079, ALS3 and UME6) showed significantly increased expression (⥠2 fold) in nrg1Î/Îarp2Î/Î cells compared to arp2Î/Î cells, while a further four genes (IHD1, CBP1, ORF19.6705 and ALS10) showed moderately increased expression between 1.5 and 2-fold. Thus, while deleting a transcriptional repressor of the filamentation program leads to de-repression of many hyphal genes, the entire regulated gene set is not de-repressed; this presumably reflects the complex interplay that different transcriptional (co-) repressors exert on the yeast-to-hyphae transition (Garcia-Sanchez et al., 2005, Kadosh & Johnson, 2005). We further found that despite the increased induction of some hyphal genes in the nrg1Î/Îarp2Î/Î mutant, a few of those genes are not as highly induced as in WT cells. One gene that was induced in both the ânrg1Î/Îarp2Î/Î vs arp2Î/Îâ and the ânrg1Î/Îarp2Î/Î vs WTâ-comparisons is UME6, a recently identified key regulator of the hyphal program (Banerjee et al., 2008, Zeidler et al., 2009). Interestingly, although constitutive over-expression of UME6 in WT cells resulted in constitutive filamentous growth even in the absence of hyphae signals (Carlisle et al., 2009), the increased expression level of UME6 in the nrg1Î/Îarp2Î/Î mutant is not sufficient to restore filamentation in the absence of a functional Arp2/3 complex. Thus despite partial de-repression of the hyphal program, hyphae do not form, making it likely other roles of the Arp2/3 complex, such as its function in actin patch formation and actin branching, are required for hyphal development.
2010-01-22 | E-GEOD-19582 | biostudies-arrayexpress