A pleiotropic role of sialidase in the pathogenicity of .

As one of the keystone pathogens of periodontitis, the oral bacterium produces an array of virulence factors, including a recently identified sialidase (PG0352). Our previous report involving loss-of-function studies indicated that PG0352 plays an important role in the pathophysiology of . However, this report had not been corroborated by gain-of-function studies or substantiated in different strains. To fill these gaps, herein we first confirm the role of PG0352 in cell surface structures (e.g., capsule) and serum resistance using W83 strain through genetic complementation and then recapitulate these studies using ATCC33277 strain. We further investigate the role of PG0352 and its counterpart (PGN1608) in ATCC33277 in cell growth, biofilm formation, neutrophil killing, cell invasion, and -induced inflammation. Our results indicate that PG0352 and PGN1608 are implicated in cell surface structures, hydrophobicity, biofilm formation, resistance to complement and neutrophil killing, and host immune responses. Possible molecular mechanisms involved are also discussed. In summary, this report underscores the importance of sialidases in the pathophysiology of and opens an avenue to elucidate their underlying molecular mechanisms.