Modulation of adhesion to biotic model surfaces by fungal lectins and protease inhibitors.

, a Gram-negative bacterium, is one of the most common causes of foodborne illness worldwide. Its adhesion mechanism is mediated by several bacterial factors, including flagellum, protein adhesins, lipooligosaccharides, proteases, and host factors, such as surface glycans on epithelial cells and mucins. Fungal lectins, specialized carbohydrate-binding proteins, can bind to specific glycans on host and bacterial cells and thus influence pathogenesis. In this study, we investigated the effects of fungal lectins and protease inhibitors on the adhesion of to model biotic surfaces (mucin, fibronectin, and collagen) and Caco-2 cells as well as the invasion of Caco-2 cells. The lectins agglutinin (MOA) and tectonin 2 (Tec2) showed remarkable efficacy in all experiments. In addition, different pre-incubations of lectins with or Caco-2 cells significantly inhibited the ability of to adhere to and invade Caco-2 cells, but to varying degrees. Pre-incubation of Caco-2 cells with selected lectins reduced the number of invasive cells the most, while simultaneous incubation showed the greatest reduction in adherent cells. These results suggest that fungal lectins are a promising tool for the prevention and treatment of infections. Furthermore, this study highlights the potential of fungi as a rich reservoir for novel anti-adhesive agents.