Sugarcoating it: Enterococcal polysaccharides as key modulators of host–pathogen interactions

Abstract

The human gastrointestinal tract (GIT) harbors a diverse microbial ecosystem that plays a critical role in defining health and disease. Members of the bacterial genus Enterococcus sp. are common gut-resident microbes that have the potential to cause life-threatening infections when GIT homeostasis is disrupted due to immunosuppression or prolonged antibiotic treatment Enterococcus faecalis and Enterococcus faecium, for instance, are predominant gut inhabitants accounting for the majority of hospital-acquired enterococcal infections The pathogenic success of enterococci is partly attributed to their intrinsic tolerance and acquired resistance to diverse antimicrobials, as well as their ability to endure and thrive in harsh environments Emerging studies suggest that this environmental persistence is in part mediated by polysaccharides Of note, Enterococcus sp. possess highly diverse glycobiological arrangements (Fig 1 ) given their ability to build not only essential structural polysaccharides, such as peptidoglycan (PG), enterococcal polysaccharide antigen (EPA), and wall teichoic acids (WTAs), but also the capacity to synthesize capsule polysaccharides (CPs), lipoteichoic acids (LTAs), and other extracellular polysaccharides These glycans play a prominent role in maintaining bacterial cell integrity and morphology in conjunction with building a dynamic interface with the environment Enterococcal polysaccharides also coordinate major host-pathogen interactions since they modulate cell adhesion and the formation of microbial multicellular communities. Further, these complex sugars have been proposed to promote GIT colonization and penetration of intestinal barriers In this review, we discuss multiple mechanisms through which polysaccharides can shape the physiology and pathogenicity of enterococci, with an especial emphasis on E. faecalis and E. faecium.