For most pathogenic bacteria, a crucial initial step in the establishment of infection is the recognition and colonization of the host tissue by specific attachment via surface-exposed adhesion molecules. In gram-negative bacteria, these adhesins are displayed on the outer membrane as single proteins (e.g. autotransporters or two-partner secretion systems) or can be incorporated into filamentous polymers (chaperone/usher pili, type II pili, type IV secretion pili and curli). Adhesin-mediated attachment can simply serve as a means of avoiding clearance through mechanical shear, or can trigger more complex host responses like cytoskeleton reorganization and cell invasion, or provide the required proximity to the host cell to enable other virulence mechanisms to come into action (e.g. effector injection through type III and type IV secretion systems). In an era of increased antibiotics resistance and difficulties in controlling hospital-acquired infections, it is essential to gain a better understanding of the fundamental principles governing the infection process. Our lab studies the structural molecular biology of bacterial adhesins and cell-surface filaments with respect to their function in bacterial pathogenesis, with the ultimate aim of developing a new generation of virulence-targeted antimicrobials.
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