Porphyromonas gingivalisdisturbs host–commensal homeostasis by changing complement function

Abstract

Porphyromonas gingivalis is a Gram-negative anaerobic rod that has been proposed as an orchestrator of complement-dependent dysbiotic inflammation. This notion was suggested from its capacities to manipulate the complement–Toll-like receptor crosstalk in ways that promote dysbiosis and periodontal disease in animal models. Specifically, while at low colonization levels, P. gingivalis interferes with innate immunity and leads to changes in the counts and composition of the oral commensal microbiota. The resulting dysbiotic microbial community causes disruption of host–microbial homeostasis, leading to inflammatory bone loss. These findings suggested that P. gingivalis can be considered as a keystone pathogen. The concept of keystone pathogens is one where their effects have community-wide significance and are disproportionate of their abundance. The present review summarizes the relevant literature and discusses whether the results from the animal models can be extrapolated to man.

Effects of Porphyromonas gingivalis LPS and LR12 peptide on TREM‐1 expression by monocytes

“…P. gingivalis is considered as a keystone pathogen in periodontitis which is a dysbiotic inflammatory disease (Olsen, Lambris, & Hajishengallis, ). The host immune response is initially subverted by major periodontopathogens helped by accessory pathogens and is overactivated by pathobionts.…”

Integrating complement into the molecular pathogenesis of Hidradenitis Suppurativa

“…[38] Microbiome studies in HS have identified the Porphyromonas and Peptinophillus species as strongly associated with disease activity, [39] particularly in the setting of dermal tunnels in HS. [42,43] These pathogens-derived proteases can also cleave cell-surface receptors such as CD14, resulting in impaired clearance of apoptotic cells and promotion of chronic inflammation. [42,43] These pathogens-derived proteases can also cleave cell-surface receptors such as CD14, resulting in impaired clearance of apoptotic cells and promotion of chronic inflammation.…”

Citrullination as a plausible link to periodontitis, rheumatoid arthritis, atherosclerosis and Alzheimer’s disease

“…P. gingivalis manipulates the host’s cellular immune responses and undermines host-microbe homeostasis [5], thereby leading to dysbiosis in a previously symbiotic microbiome [2]. Breakdown of cellular barriers allows dissemination of this pathogen to the rest of the body.…”