Abstract
Periodontitis is a common intraoral infection and is inextricably linked to systemic diseases. Recently, the regulation between host immunologic response and periodontal pathogens has become a hotspot to explain the mechanism of periodontitis and related systemic diseases. Since Porphyromonas gingivalis (P. gingivalis) was proved as critical periodontal pathogen above all, researches focusing on the mechanism of its virulence factors have received extensive attention. Studies have shown that in the development of periodontitis, in addition to the direct release of virulent factors by periodontal pathogens to destroy periodontal tissues, over-low or over-high intrinsic immune and inflammatory response mediated by Toll-like receptors (TLRs) can lead to more lasting destruction of periodontal tissues. It is very necessary to sort out how various cytopathic factors of P. gingivalis mediate inflammation and immune responses between the host through TLRs so as to help precisely prevent, diagnose, and treat periodontitis in clinic. This review summarizes the role of three most widely studied pathogenic factors produced by P. gingivalis (lipopolysaccharide, gingipains, pili) and their interactions with TLRs at the cellular and molecular level in the progress of periodontitis.
Highlights
Periodontitis refers to inflammatory pathological damage of the gums and periodontal support tissues, including the gums, alveolar bone, periodontal ligament, and cementum
Previous research reported that the mediation of TLR2 is essential for the loss of alveolar bone caused by P. gingivalis in animal models, and treatment of E. coli-LPS-tolerant bone marrowderived macrophages (BMDM) with P. gingivalis resulted in upregulation of TLR2 expression and excessive tumor necrosis factor (TNF) production in vitro (Papadopoulos et al, 2013)
Due to the common features and functional interrelationship of MD-1/CD180 and TLR4/MD-2, the LPS-originating pathway can be restrained by MD-1/CD180 acting as an MD-2/TLR4 antagonist, which occurs in a wide ranges of cell types, including human embryonic kidney 293 (HEK293) cells, dendritic cells, and macrophages (Divanovic et al, 2005)
Summary
Periodontitis refers to inflammatory pathological damage of the gums and periodontal support tissues, including the gums, alveolar bone, periodontal ligament, and cementum. For. TLR-Mediated Immune Responses of Porphyromonas gingivalis example, animal experiments have been used to demonstrate that P. gingivalis can colonize some distant organs, such as the coronary artery, placenta, liver, and even the brain, causing specific infections associated with the activation of Tolllike receptors (TLRs) (Olsen and Yilmaz, 2016; Huck et al, 2018). TLR-Mediated Immune Responses of Porphyromonas gingivalis example, animal experiments have been used to demonstrate that P. gingivalis can colonize some distant organs, such as the coronary artery, placenta, liver, and even the brain, causing specific infections associated with the activation of Tolllike receptors (TLRs) (Olsen and Yilmaz, 2016; Huck et al, 2018) Based on these data, an increasing number of scholars are investing in molecular biology to explore the pathogenic mechanisms of P. gingivalis (Olsen et al, 2018). This review focuses on how three critical P. gingivalis pathogenic factors explicitly contribute to the pathogenesis of periodontitis and how they mediate innate immunoinflammatory host responses via different TLRs
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