His presentation highlighted the research carried out at the INBr laboratory on the formation mechanisms of genotoxic compounds during the thermal processing of foods, an important challenge for food quality and food safety.

A great recognition of our research on the international stage!

Cerckel G, Dereinne D, Ledesma-García L, Meuric V, Desguin B, Mignolet J, Soumillion P, and Hols P (2026) Non-peptide dysbiosis metabolites reprogram a peptide quorum-sensing receptor to induce sustained predation in beneficial streptococci. PLoS Biol 24(3): e3003718. https://doi.org/10.1371/journal.pbio.3003718

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Staphylococcus aureus colonizes the human skin, thereby causing various disorders, including eczema. Highly virulent strains that are resistant to multiple antibiotics represent a leading cause of nosocomial infections that are difficult to eradicate, emphasizing the need for alternative treatments. 

Attachment of S. aureus to the skin involves specific bacterial cell surface proteins that bind to target ligands on the outer surface of the epidermis. In a recent study published in Science Advances, research teams from Auburn University, University of Birmingham, and UCLouvain used in vitro and in silico single-molecule force spectroscopy to demonstrate that the staphylococcal serine-aspartate repeat D (SdrD) protein forms ultrastrong bonds with the skin protein desmoglein-1 (DSG-1). 
This is among the strongest non-covalent protein-protein interaction ever reported, explaining why the pathogen remains attached to the skin even after scratching or washing, and helping us understand why these infections are so difficult to get rid of. 

Remarkably, the teams discovered that calcium, an element better known for strengthening bones, plays a key role in fortifying this bacterial grip. 
When calcium levels are reduced, the bond between SdrD and DSG-1 weakens significantly. When calcium is added back, the bond becomes even stronger. This finding is particularly relevant for patients with eczema, where disrupted calcium gradients amplify SdrD interactions, which could potentially intensify S. aureus virulence. 

This study provides crucial insights into the calcium-dependent regulation of pathogen adhesion and opens the door to new strategies for combating antibiotic-resistant infections. Instead of trying to kill bacteria directly, which often drives the evolution of resistance, scientists could design therapies that block or weaken bacterial adhesion.