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As phages are extensively investigated as novel therapy tools but also as transfer agents for antibiotic resistance genes, thorough understanding of phage—host interactions becomes crucial. Prerequisite for phage infection is its adhesion to the host surface. Herein, we used atomic force microscopy-based single-particle force spectroscopy with phage-decorated tips to decipher the adhesion of phage 187 on living Staphylococcus aureus cells. We found that addition of free N-acetyl-D-glucosamine was able to decrease phage adhesion, suggesting that this monosaccharide plays major role in phage 187 infection of S. aureus. Moreover, phage 187 adhesion on monosaccharide-coated model surfaces combined with plaque forming unit counts suggested that a direct link can be established between the propensity to bind to a saccharide and the capability of the latter to inhibit phage infection. On a nanoscale level, single-particle force spectroscopy was successfully used to identify a major receptor required for phage 187 infection of S. aureus but also evidenced that this receptor was responsible for phage adhesion on host-cells. Our work demonstrates that single-particle force spectroscopy is a powerful platform to screen and predict the molecular target of phages on their host surfaces. [ABSTRACT FROM AUTHOR]

Enterohaemorrhagic Escherichia coli (EHEC) are bacterial pathogens responsible for life-threatening diseases in humans, such as hemolytic and uremic syndrome. It has been previously demonstrated that the interplay between EHEC and nitric oxide (NO), a mediator of the host immune innate response, is critical for infection outcome, since NO affects both Shiga toxin (Stx) production and adhesion to enterocytes. In this study, we investigated the role of the NO reductase NorVW in the virulence and fitness of two EHEC strains in a murine model of infection. We determined that the deletion of norVW in the strain O91:H21 B2F1 has no impact on its virulence, whereas it reduces the ability of the strain O157:H7 620 to persist in the mouse gut and to produce Stx. We also revealed that the fitness defect of strain 620 ΔnorVW is strongly attenuated when mice are treated with an NO synthase inhibitor. Altogether, these results demonstrate that the NO reductase NorVW participates in EHEC resistance against NO produced by the host and promotes virulence through the modulation of Stx synthesis. The contribution of NorVW in the EHEC infectious process is, however, strain-dependent and suggests that the EHEC response to nitrosative stress is complex and multifactorial. [ABSTRACT FROM AUTHOR]