Manipulation of Neutrophils by Porphyromonas gingivalis in the Development of Periodontitis

Abstract

The pathogenesis of the chronic periodontal disease is associated with a skewed host inflammatory response to periodontal pathogens, such as Porphyromonas gingivalis, that accounts for the majority of periodontal tissue damage. Neutrophils are the most abundant leukocytes in periodontal pockets and depending on the stage of the disease, also plentiful PMNs are present in the inflamed gingival tissue and the gingival crevice. They are the most efficient phagocytes and eliminate pathogens by a variety of means, which are either oxygen-dependent or -independent. However, these secretory lethal weapons do not strictly discriminate between pathogens and host tissue. Current studies describe conflicting findings about neutrophil involvement in periodontal disease. On one hand literature indicate that hyper-reactive neutrophils are the main immune cell type responsible for this observed tissue damage and disease progression. Deregulation of neutrophil survival and functions, such as chemotaxis, migration, secretion of antimicrobial peptides or enzymes, and production of reactive oxygen species, contribute to observed tissue injury and the clinical signs of periodontal disease. On the other hand neutrophils deficiencies in patients and mice also result in periodontal phenotype. Therefore, P. gingivalis represents a periodontal pathogen that manipulates the immune responses of PMNs, employing several virulence factors, such as gingipains, serine proteases, lipid phosphatases, or fimbriae. This review will sum up studies devoted to understanding different strategies utilized by P. gingivalis to manipulate PMNs survival and functions in order to inhibit killing by a granular content, prolong inflammation, and gain access to nutrient resources.

The Msp Protein of Treponema denticola Interrupts Activity of Phosphoinositide Processing in Neutrophils

“…T. denticola is known to play a suppressive role in immune cells compared to other members of the red complex which readily activate neutrophils and trigger increases in gene transcription (49)(50)(51)(52)(53). Based on this observation, which was supported by the results in Fig.…”

Genomewide Association Study Identifies Cxcl Family Members as Partial Mediators of LPS-Induced Periodontitis

“…To further characterize differences between A/J, a low bone loss strain, and C57BL/6J, a high bone loss strain, tissue specimens were analyzed for immune and pro‐inflammatory cellular markers through immunohistochemistry (IHC) staining. Neutrophil and T cells were assessed in A/J and C57BL/6J mice after LPS treatment because neutrophils and T cells are known to infiltrate into periodontal lesions in response to infection and inflammation . When comparing control groups, there was no difference in immunostaining between C57BL/6J control and A/J control groups for both neutrophils and T cells.…”

Morphological characterization of para‐ and proinflammatory neutrophil phenotypes using transmission electron microscopy

“…These phagosomes show engulfed bacteria that have not yet been digested. It was previously demonstrated that periodontal pathogens such as P. gingivalis can inhibit phagocytosis by using microbial factors such as gingipains therefore, it is interesting that the health associated S. oralis , in contrast, induced phagocytosis in the naïve cells.…”