Abstract
Streptococcus suis is a Gram-positive bacterium, which causes sepsis and meningitis in pigs and humans. This review examines the role of known S. suis virulence factors in adhesion and S. suis carbohydrate-based adhesion mechanisms, as well as the inhibition of S. suis adhesion by anti-adhesion compounds in in vitro assays. Carbohydrate-binding specificities of S. suis have been identified, and these studies have shown that many strains recognize Galα1-4Gal-containing oligosaccharides present in host glycolipids. In the era of increasing antibiotic resistance, new means to treat infections are needed. Since microbial adhesion to carbohydrates is important to establish disease, compounds blocking adhesion could be an alternative to antibiotics. The use of oligosaccharides as drugs is generally hampered by their relatively low affinity (micromolar) to compete with multivalent binding to host receptors. However, screening of a library of chemically modified Galα1-4Gal derivatives has identified compounds that inhibit S. suis adhesion in nanomolar range. Also, design of multivalent Galα1-4Gal-containing dendrimers has resulted in a significant increase of the inhibitory potency of the disaccharide. The S. suis adhesin binding to Galα1-4Gal-oligosaccharides, Streptococcal adhesin P (SadP), was recently identified. It has a Galα1-4Gal-binding N-terminal domain and a C-terminal LPNTG-motif for cell wall anchoring. The carbohydrate-binding domain has no homology to E. coli P fimbrial adhesin, which suggests that these Gram-positive and Gram-negative bacterial adhesins recognizing the same receptor have evolved by convergent evolution. SadP adhesin may represent a promising target for the design of anti-adhesion ligands for the prevention and treatment of S. suis infections.
Highlights
Streptococcus suis is a Gram-positive bacterium, which is an emerging cause of serious infections, such as meningitis, septicemia, endocarditis and pneumonia in pigs and zoonotic meningitis in humans [1±4]
Adhesion to the capillary endothelial cells precedes the penetration of S. suis into the brain from blood circulation and could be mediated by either direct invasion of bacteria into the cells by endocytic mechanisms or by disrupting the cell junctions
Studies characterizing gene expression upon bacterial contact with endothelial cells have revealed that the mRNA levels of signal peptidase and sortase E involved in pilus synthesis were increased [65]. This suggests that, with the so far unknown mechanisms, S. suis can sense the contact with host cells and induce the expression of genes important for interaction with host cells
Summary
Streptococcus suis is a Gram-positive bacterium, which is an emerging cause of serious infections, such as meningitis, septicemia, endocarditis and pneumonia in pigs and zoonotic meningitis in humans [1±4]. Host- and tissue-specific adhesion of both the Gram-negative and Gram-positive bacteria is a prerequisite for infection and invasive disease [6,7]. Bacteria have evolved multiple adhesins to recognize host cell surface carbohydrate and protein receptors [8]. Anti-adhesion therapy is based on the inhibition of bacterial attachment to a specific receptor structure [10,11]. An advantage of the prevention of infections by receptor analogs could be that bacteria do not develop resistance, in contrast to the traditional bactericidal drugs. Since anti-adhesive compounds target adhesins, which are required for a specific colonization of the host, the mutant phenotypes of bacteria deficient in adhesion would be eliminated by the host. S. suis adhesion mechanisms that are based on the recognition of carbohydrate receptors, as well as the development of carbohydrate-based anti-adhesive compounds are reviewed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
