Implication of immune interactions in bacterial virulence: is Porphyromonas gingivalis an “Invader” or “Stealth Element” in periodontal lesions?

Abstract

Porphyromonas gingivalis (Pg), a Gram-negative anaerobic blackpigmented rod bacterium, has been recognized as the most potent etiologic bacterium in human chronic periodontitis. It possesses a variety of putative virulence factors providing both tissue destruction and host evasion including lipopolysaccharides (LPS), fimbriae, various proteinases, etc. These factors actively participate in periodontal tissue destruction. However, recent evidence suggests that Pg has also evolved mechanisms to inhibit or confuse host immune systems. Thus, Pg is suggested to behave not only like an “active invader”, but also like a “stealth element” in periodontal lesions. In the present study, repeated exposure of Pg components induced tolerance resulting in selective inhibition of cytokine production of both monocytes and gingival fibroblasts in a different fashion from that described for LPS in Escherichia coli. It was also revealed that Pg LPS induced a unique dendritic cell subset with a CD14⁺CD16⁺ phenotype that exhibited weak maturation. In animal studies, administration of live Pg or its LPS exerted a regulatory effect on systemic markers such as triglycerides or adiponectin. Taken together, these findings suggest that Pg may be able to adapt to the local immune defense, contributing to the connection between systemic and periodontal disease.