A pleiotropic role of sialidase in the pathogenicity of Porphyromonas gingivalis .
Christopher PhamShuaiqi GuoXiao HanLaurynn ColemanChing Wooen SzeHuizhi WangJun LiuChunhao LiPublished in: Infection and immunity (2024)
As one of the keystone pathogens of periodontitis, the oral bacterium Porphyromonas gingivalis 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 P. gingivalis . However, this report had not been corroborated by gain-of-function studies or substantiated in different P. gingivalis strains. To fill these gaps, herein we first confirm the role of PG0352 in cell surface structures (e.g., capsule) and serum resistance using P. gingivalis W83 strain through genetic complementation and then recapitulate these studies using P. gingivalis 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 P. gingivalis -induced inflammation. Our results indicate that PG0352 and PGN1608 are implicated in P. gingivalis 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 P. gingivalis and opens an avenue to elucidate their underlying molecular mechanisms.
Keyphrases
- biofilm formation
- pseudomonas aeruginosa
- cell surface
- staphylococcus aureus
- escherichia coli
- candida albicans
- immune response
- oxidative stress
- high resolution
- high throughput
- toll like receptor
- gene expression
- genome wide
- inflammatory response
- endothelial cells
- mass spectrometry
- multidrug resistant
- high glucose
- high density