Antimicrobial Resistance (AMR) is one of the most pressing global health threats of our time, demanding immediate and innovative solutions. Our research focuses on the virulence proteins that bacteria use as their molecular arsenal to cause disease. By combining structural biology with advanced molecular and biochemical techniques, we are uncovering the intricate mechanisms behind key bacterial virulence factors.
At the heart of our work lies the Type V secretion system, responsible for secreting autotransporters—the largest group of secreted proteins in Gram-negative bacteria [1]. These proteins play crucial roles in pathogenesis, including promoting bacterial aggregation and biofilm formation, along with facilitating adherence to host cells, and causing cytotoxicity.
Our multidisciplinary approach that combines X-ray crystallography, biophysical techniques, immunoassays, and cellular assays, has allowed us to elucidate the structure and function of diverse autotransporter proteins, including adhesins and cytotoxins, revealing how they facilitate their pathogenic functions [2-5]. For example, our findings indicate that different autotransporter adhesins promote bacterial aggregation and biofilm formation through a conserved self-association mechanism, facilitating host colonization and bacterial persistence in various environmental niches [2-3]. We are also uncovering, in atomic detail, how autotransporter toxins such as the proteases Ssp and EspC invade host cells to cause cytotoxic damage.
This understanding is enabling us to develop antimicrobials that "disarm rather than kill bacteria," a novel strategy aimed at minimising resistance development. We are actively creating autotransporter inhibitors, including our patented biofilm blocker [6], which can serve as stand-alone antibiofilm therapy or enhance the efficacy of failing antibiotics. We are also developing molecules that block autotransporter toxins laying the groundwork for future anti-toxin drugs.
Overall, our research not only provides a deeper understanding of bacterial pathogenesis but also opens new avenues for combating AMR.