Pathogenesis of Fungal Biofilms in Different Environmental Conditions and Clinical Outcomes

Fungi can grow as complex cellular communities that adhere strongly to the surfaces or tissues, called biofilms. Aspergillus, Candida, Cryptococcus, dermatophytes, dimorphic fungi, Pneumocystis and Trichosporon are some medically important fungi that may produce biofilms. Although most biofilms can be formed on abiotic surfaces, fungal biofilms have been reported in the human host on tooth surfaces, lungs and tissues of respiratory airway tract, urinary tract and eyes. A complex network involving multiple environmental factors (availability of nutrients and/or oxygen, temperature, pH) and fungal adaptation mechanisms (transporters, enzyme and detoxifiers production, wall remodeling, phenotypic switching) contribute to fungal biofilm formation. In the clinical setting, fungal biofilms have been associated with an increase in device-related infections and they can also raise the risk of the invasion, persistence and severity of infections. Furthermore, because of their structural complexity, the presence of extracellular matrix, metabolic heterogeneity and the induced genes expression for efflux pumps, the biofilms are highly resistant to both antifungal drugs and human host defenses.

Knowing the mechanisms by which fungi form biofilm, despite environmental adversity or the human host's responsiveness mechanisms (immune complex system with phagocytic cells, production of cytokines and immune molecules that trigger different forms of response to stress) is an area of significant research interest and practical importance.

Thus, this Research Topic intends to contribute to the understanding of the role of biofilm in different conditions, biotic and abiotic, as well as new strategies supported by in vivo or ex vivo studies, highlighting the emerging segmentation of biofilm technologies and provide a justification for multi-target therapies designed to disrupt the biofilm microenvironment complex.

This Research Topic does not consider submissions of descriptive studies based on amplicon profiles (e.g. 16S rRNA gene) lacking a clear hypothesis and/or failing to provide new insight into the microbial interactions being studied.