Innovative Approaches to Counteract Bacterial Virulence and Biofilm

The research group works in the field of clinical microbiology, with a focus on the phenotypic and genetic aspects of bacterial virulence and biofilm-formation in bacterial human pathogens and their role in infection pathogenesis and host–microbe interactions.

Biofilm-associated lifestyles are known for their high tolerance to external stress, which often renders conventional antibiotic or biocide treatments ineffective.

Bacterial virulence factors - comprising adhesive structures, secreted toxins and enzymes, immune-evasion molecules, nutrient-acquisition systems and regulatory networks - play a central role in enabling pathogens to colonize hosts, overcome host defenses, and cause disease.

Research addresses both the molecular identification and functional characterization of these virulence determinants, exploring their interplay with host and environmental factors in complex infection settings.

Experimental activities include the study and development of innovative strategies for preventing and treating biofilm formation. The team investigates non-biocidal compounds inhibiting specific virulence factors in pathogenic bacteria, aiming to counteract virulence rather than bacterial growth, thereby reducing the risk of resistance selection.

The group also develops new experimental models to compare the phenotypical characteristics of planktonic and sessile bacterial on various biomaterials under different growth conditions. Additional efforts focus on testing new physicochemical methods to detach sessile bacteria, exploring genetic approaches, evaluating experimental molecules of synthetic or natural origin, and assessing innovative materials that inhibit microbial adhesion on both abiotic surfaces and eukaryotic cells or interfere with bacterial virulence.

Understanding these mechanisms is pivotal not only for pathogenesis elucidation, but also to identify anti-virulence therapies that target pathogenic potential rather than bacterial viability and thus may reduce selective pressure for resistance.

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