Candida albicans biofilms: development, regulation, and molecular mechanisms

Gulati, Megha; Nobile, Clarissa J.

doi:10.1016/j.micinf.2016.01.002

Cited by 536 publications

(487 citation statements)

References 77 publications

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“…2). As hyphae formation plays a vital role in C. albicans biofilm formation (Lu et al ., 2014; Gulati and Nobile, 2016), the strategies to target morphological transition and biofilm development may be closely interlinked.…”

Section: Discussionmentioning

confidence: 99%

(1‐aryloxy‐2‐hydroxypropyl)‐phenylpiperazine derivatives suppress Candida albicans virulence by interfering with morphological transition

Zhao

Huang

Sun

et al. 2018

Microbial Biotechnology

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SummaryClinical treatment of Candida albicans infections has become more difficult due to the limited development of antifungal agents and the rapid emergence of drug resistance. In this study, we demonstrate the synthesis of a series of piperazine derivatives and the evaluation of their inhibitory activity against C. albicans virulence. Thirty‐four (1‐aryloxy‐2‐hydroxypropyl)‐phenylpiperazine derivatives, including 25 new compounds, were synthesized and assessed for their efficacy against the physiology and pathogenesis of C. albicans. Several compounds strongly inhibited the morphological transition and virulence of C. albicans cells, although they did not influence the growth rate of the fungal pathogen. A leading novel compound, (1‐(4‐ethoxyphenyl)‐4‐(1‐biphenylol‐2‐hydroxypropyl)‐piperazine), significantly attenuated C. albicans virulence by interfering with the process of hyphal development, but it showed no cytotoxicity against human cells at a micromolar level. These findings suggest that (1‐aryloxy‐2‐hydroxypropyl)‐phenylpiperazine derivatives could potentially be developed as novel therapeutic agents for the clinical treatment of C. albicans infections by interfering with morphological transition and virulence.

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Section: Discussionmentioning

confidence: 99%

(1‐aryloxy‐2‐hydroxypropyl)‐phenylpiperazine derivatives suppress Candida albicans virulence by interfering with morphological transition

Zhao

Huang

Sun

et al. 2018

Microbial Biotechnology

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“…Once formed, these biofilms are resistant to antifungal drugs and also serve as reservoirs that can seed disseminated (nonbiofilm) infections. On the basis of a series of in vitro and in vivo studies, C. albicans biofilm development has been divided into four stages: (i) adherence to a surface, (ii) proliferation on the surface, (iii) maturation into a complex biofilm, and (iv) dispersion of cells from the biofilm to seed new niches (for reviews, see references [1][2][3][4][5].…”

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confidence: 99%

Assessment and Optimizations of Candida albicans In Vitro Biofilm Assays

Lohse

Gulati

Arevalo

et al. 2017

Antimicrob Agents Chemother

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Candida albicans biofilms have a significant medical impact due to their rapid growth on implanted medical devices, their resistance to antifungal drugs, and their ability to seed disseminated infections. Biofilm assays performed in vitro allow for rapid, high-throughput screening of gene deletion libraries or antifungal compounds and typically serve as precursors to in vivo studies. Here, we compile and discuss the protocols for several recently published C. albicans in vitro biofilm assays. We also describe improved versions of these protocols as well as novel in vitro assays. Finally, we consider some of the advantages and disadvantages of these different types of assays.

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“…The highly structured biofilms were constructed on crisscrossing hyphae; thus, interruption of the yeast-to-hypha transition would prevent biofilm development (7,8). The filamentation assay showed that EE obviously inhibited the morphological transition (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Candida albicans, the main pathogenic agent responsible for candidiasis, is able to transform from budding yeasts to cells with filamentous growth and, eventually, cells that form biofilms (5,6). C. albicans biofilm formation exacerbates clinical infections by forming a reservoir for producing recalcitrant pathogenic cells, which can act as seeds to disseminate the organism to the bloodstream, leading to invasive systemic infections of tissues and organs (7). In addition, biofilm cells display phenotypic traits that are dramatically different from those of their planktonic counterparts, resulting in enhanced resistance to antifungal drugs (7,8).…”

mentioning

confidence: 99%

“…C. albicans biofilm formation exacerbates clinical infections by forming a reservoir for producing recalcitrant pathogenic cells, which can act as seeds to disseminate the organism to the bloodstream, leading to invasive systemic infections of tissues and organs (7). In addition, biofilm cells display phenotypic traits that are dramatically different from those of their planktonic counterparts, resulting in enhanced resistance to antifungal drugs (7,8). Studies have shown that azoles are ineffective against C. albicans biofilms due to the upregulation of efflux pumps in biofilms (9), while conventional amphotericin B failed to reach biofilm cells because of the enhanced extracellular matrix or beta-glucan synthesis during biofilm growth (10).…”

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confidence: 99%

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In Vitro Antibiofilm Activity of Eucarobustol E against Candida albicans

Liu

Shang

et al. 2017

Antimicrob Agents Chemother

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Formyl-phloroglucinol meroterpenoids (FPMs) are important types of natural products with various bioactivities. Our antifungal susceptibility assay showed that one of the Eucalyptus robusta-derived FPMs, eucarobustol E (EE), exerted a strong inhibitory effect against Candida albicans biofilms at a concentration of 16 g/ml. EE was found to block the yeast-to-hypha transition and reduce the cellular surface hydrophobicity of the biofilm cells. RNA sequencing and real-time reverse transcription-PCR analysis showed that exposure to 16 g/ml of EE resulted in marked reductions in the levels of expressions of genes involved in hyphal growth (EFG1, CPH1, TEC1, EED1, UME6, and HGC1) and cell surface protein genes (ALS3, HWP1, and SAP5). Interestingly, in response to EE, genes involved in ergosterol biosynthesis were downregulated, while the farnesol-encoding gene (DPP3) was upregulated, and these findings were in agreement with those from the quantification of ergosterol and farnesol. Combined with the obvious elevation of negative regulator genes (TUP1, NRG1), we speculated that EE's inhibition of carbon flow to ergosterol triggered the mechanisms of the negative regulation of hyphal growth and eventually led to biofilm inhibition.

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Candida albicans biofilms: development, regulation, and molecular mechanisms

Cited by 536 publications

References 77 publications

(1‐aryloxy‐2‐hydroxypropyl)‐phenylpiperazine derivatives suppress Candida albicans virulence by interfering with morphological transition

(1‐aryloxy‐2‐hydroxypropyl)‐phenylpiperazine derivatives suppress Candida albicans virulence by interfering with morphological transition

Assessment and Optimizations of Candida albicans In Vitro Biofilm Assays

In Vitro Antibiofilm Activity of Eucarobustol E against Candida albicans

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