Cited by 104Antifungal resistance and susceptibilityBacterial biofilms and quorum sensingFungal and yeast genetics research

Role of matrix β-1,3 glucan in antifungal resistance of non-albicans Candida biofilms

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Mitchell, K. F., Taff, H. T., Cuevas, M. A., Reinicke, E. L., Sanchez, H., Andes, D. R.·2013·Antimicrobial Agents and Chemotherapy

Abstract

Candida biofilm infections pose an increasing threat in the health care setting due to the drug resistance associated with this lifestyle. Several mechanisms underlie the resistance phenomenon. In Candida albicans, one mechanism involves drug impedance by the biofilm matrix linked to β-1,3 glucan. Here, we show this is important for other Candida spp. We identified β-1,3 glucan in the matrix, found that the matrix sequesters antifungal drug, and enhanced antifungal susceptibility with matrix β-1,3 glucan hydrolysis.

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Crossref · 10.1128/aac.02378-12

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  • C. glabrata biofilms display antifungal resistance and are characterized by a compact dense structure of yeast cells nested in an extracellular matrix composed of high levels of proteins and carbohydrates including β-1,3 glucan.

    “C. glabrata biofilms display antifungal resistance, and are characterized by a compact dense structure of yeast cells nested in an extracellular matrix which is composed of high levels of proteins and carbohydrates including β-1,3 glucan [50,51,52].”

    From Candida glabrata: A Lot More Than Meets the Eye (2019) · cites this paper as [52]

  • Biofilms prevent, to a greater or lesser extent, antifungal drug penetration through a diffusion barrier that acts as an ion-exchange resin binding charged antibiotic molecules, contributing to biofilm drug resistance including in C. glabrata.

    “It is thought that biofilms prevent, to a greater or lesser extent, the penetration of antifungal drugs through their structure, by the establishment of a diffusion barrier, which acts as an ion-exchange resin, binding charged antibiotic molecules, contributing to biofilm drug resistance, including in the case of C. glabrata [44,150,155].”

    From Candida glabrata Biofilms: How Far Have We Come? (2017) · cites this paper as [155]

  • Disruption of β-1,3-glucans or β-1,3-glucanase treatment increases biofilm susceptibility to fluconazole, and addition of exogenous β-1,3 glucans increases fluconazole resistance in planktonic cells.

    “When induced, the disruption of β-1,3-glucans or a β-1,3-glucanase treatment have been shown to increase susceptibility of biofilms to fluconazole and the addition of exogenous β-1,3 glucans has been demonstrated to result in the rise of resistance to fluconazole in planktonic cells [155].”

    From Candida glabrata Biofilms: How Far Have We Come? (2017) · cites this paper as [155]

  • Treatment of biofilms with β-1,3-glucanase increases the susceptibility of biofilms to fluconazole, and addition of exogenous β-1,3-glucans increases the tolerance of planktonic cells to fluconazole.

    “Thus, treatment of biofilms with β-1,3-glucanase increases the susceptibility of biofilms to fluconazole (130), and addition of exogenous β-1,3-glucans increases the tolerance of planktonic cells to fluconazole (122).”

    From <i>Candida albicans</i> Biofilms and Human Disease (2015) · cites this paper as [122]

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Authors
Mitchell, K. F., Taff, H. T., Cuevas, M. A., Reinicke, E. L., Sanchez, H., & Andes, D. R.
Affiliations
  • University of Wisconsin–Madison (US)
  • University of Puerto Rico at Cayey (PR)
  • University of Wisconsin, Madison, Wisconsin, USA
Venue
Antimicrobial Agents and Chemotherapy
Published
2013-04
Volume
57
Issue
4
Pages
1918-1920
ISSN
  • 0066-4804 (ISSN-L)
  • 1098-6596
OpenAlex
W2122010658
Cited by
104
References
24
Citations by year
2026: 6 · 2025: 4 · 2024: 4 · 2023: 7 · 2022: 8 · 2021: 4 · 2020: 7 · 2019: 9 · 2018: 5 · 2017: 15 · 2016: 10 · 2015: 11 · 2014: 10 · 2013: 4
FWCI
8.42
Type
journal article
Language
en
Open access
Locations
  • Antimicrobial Agents and Chemotherapy (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of General Medical Sciences (T32GM008692)
  • National Institute of Allergy and Infectious Diseases (NIH R01 AI073289-01, R01AI073289)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Keywords
β-1,3-glucan, Candida biofilms, non-albicans Candida, antifungal resistance, biofilm matrix, antifungal susceptibility, glucan hydrolysis
MeSH terms
Antifungal Agents, Candida albicans, Proteoglycans, Biofilms, Drug Resistance, Fungal, beta-Glucans

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