Biofilm Dynamics in Fungal Pathogens

Fungal biofilms represent structured communities in which cells adhere to surfaces and to each other, enveloped within a self-produced extracellular matrix. These dynamic assemblies undergo sequential phases—initial attachment, microcolony formation, maturation and dispersion—each regulated by environmental cues and intracellular signalling. Within biofilms, yeast and hyphal forms coexist, generating architectural heterogeneity that enhances resilience. The extracellular matrix, composed of polysaccharides, proteins and extracellular nucleic acids, both shields resident cells from antifungal agents and modulates host immune recognition. Transcriptional networks orchestrate morphogenetic transitions and metabolic reprogramming, enabling adaptation to nutrient limitation, pH changes and shear forces. Quorum-sensing molecules further coordinate communal behaviour, triggering dispersion of progeny cells poised to colonise new sites. Clinically, fungal biofilms on medical devices or mucosal surfaces underlie persistent infections and elevate treatment failure and mortality rates. Advances in microscopy and omics technologies continue to unravel the interconnected regulatory circuits and biophysical properties of biofilms, informing the design of novel antifungal strategies, surface coatings and diagnostic tools. Understanding biofilm dynamics in fungal pathogens is therefore critical to reducing the global burden of device‐associated and systemic mycoses.

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Biofilm Dynamics in Fungal Pathogens publication trend

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Technical terms

Biofilm: A surface-associated microbial community encased in a self-secreted matrix.

Extracellular matrix (ECM): A composite of polysaccharides, proteins and nucleic acids that embeds biofilm cells.

Planktonic: Referring to individual, free-floating microbial cells rather than those in a biofilm.

Hypha: A filamentous fungal cell type involved in adhesion and biofilm architecture.

Protease-activatable prodrug: A therapeutic precursor that releases its active agent upon cleavage by pathogen-specific proteases.

References

1. Activatable prodrug for controlled release of an antimicrobial peptide via the proteases overexpressed in Candida albicans and Porphyromonas gingivalis. Theranostics (2024).
2. Metabolic reprogramming during Candida albicans planktonic-biofilm transition is modulated by the transcription factors Zcf15 and Zcf26. PLOS Biology (2024).
3. Complexation of fungal extracellular nucleic acids by host LL-37 peptide shapes neutrophil response to Candida albicans biofilm. Frontiers in Immunology (2024).