Abstract
Glycobiology is important for the periodontal pathogen Tannerella forsythia, affecting the bacterium’s cellular integrity, its life-style, and virulence potential. The bacterium possesses a unique Gram-negative cell envelope with a glycosylated surface (S-) layer as outermost decoration that is proposed to be anchored via a rough lipopolysaccharide. The S-layer glycan has the structure 4‑MeO-b-ManpNAcCONH2-(1→3)-[Pse5Am7Gc-(2→4)-]-b-ManpNAcA-(1→4)-[4-MeO-a-Galp-(1→2)-]-a-Fucp-(1→4)-[-a-Xylp-(1→3)-]-b-GlcpA-(1→3)-[-b-Digp-(1→2)-]-a-Galp and is linked to distinct serine and threonine residues within the D(S/T)(A/I/L/M/T/V) amino acid motif. Also several other Tannerella proteins are modified with the S‑layer oligosaccharide, indicating the presence of a general O‑glycosylation system. Protein O‑glycosylation impacts the life-style of T. forsythia since truncated S-layer glycans present in a defined mutant favor biofilm formation. While the S‑layer has also been shown to be a virulence factor and to delay the bacterium's recognition by the innate immune system of the host, the contribution of glycosylation to modulating host immunity is currently unraveling. Recently, it was shown that Tannerella surface glycosylation has a role in restraining the Th17-mediated neutrophil infiltration in the gingival tissues. Related to its asaccharolytic physiology, T. forsythia expresses a robust enzymatic repertoire, including several glycosidases, such as sialidases, which are linked to specific growth requirements and are involved in triggering host tissue destruction. This review compiles the current knowledge on the glycobiology of T. forsythia.
Highlights
In our laboratory we focused the efforts on the characterization of the glycoproteome of T. forsythia
T. forsythia is a Gram-negative oral pathogen for which sialic acid is a key growth factor that may be crucial for its physiology in vivo
Those factors that are associated with the bacterial cell envelope and/or exposed to the environment are prime candidates for mediating virulence through their direct involvement in pathogen-host interactions
Summary
It has been estimated that nearly 700 bacterial taxa, phylotypes and species can colonize the oral cavity of humans [1]. Many of them trigger periodontal diseases which are multifactorial infections implicating interactions with host tissues and cells. These may lead to destruction of the periodontal structures, including the tooth-supporting tissues, alveolar bone, and periodontal ligament [2]. The link between oral microbial communities with the change from health to disease was investigated, leading to a classification of the microbiota into bacterial consortia (‘complexes‘) that occur together and are associated with the sequence of colonization on the tooth surface as well as with disease severity [5,6,7]. The ‘red complex’, which has been classified as a late colonizer in multispecies biofilm development, comprises species that are considered periodontal pathogens [4]; these are Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia
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