Porphyromonas gingivalis Mfa1 fimbria putatively binds to TLR2 and induces both IL-6 and IL-8 production in human bronchial epithelial cells

Takahashi, Yuwa; Cueno, Marni E.; Kamio, Noriaki; Iinuma, Toshimitsu; Hasegawa, Yoshiyuki; Imai, Kenichi

doi:10.1016/j.bbrc.2021.12.003

Cited by 10 publications

(8 citation statements)

References 31 publications

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“…P. gingivalis is strongly associated with various systemic diseases and bears surface components that can attach to host cells [ 2 ]. The P. gingivalis surface components fimbriae (Mfa1, FimA) and LPS are recognized by TLR2 and through downstream signaling [ 31 , 32 ]. Particularly, LPS derived from P. gingivalis (PgLPS) is a strong modulator of the immune response [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of Geniposidic Acid on Porphyromonas gingivalis-Induced Periodontitis in Mice

et al. 2022

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Periodontal disease is predominantly caused by the pathogenic bacterium Porphyromonas gingivalis that produces inflammation-inducing factors in the host. Eucommia ulmoides is a plant native to China that has been reported to reduce blood pressure, promote weight loss, and exhibit anti-inflammatory effects. Geniposidic acid (GPA) is the major component of E. ulmoides. Herein, we investigated the effects of GPA on P. gingivalis-induced periodontitis by measuring the inflammatory responses in human gingival epithelial cells (HGECs) after P. gingivalis stimulation and GPA addition in a P. gingivalis-induced periodontitis mouse model. We found that GPA addition suppressed interleukin (IL)-6 mRNA induction (33.8% suppression), IL-6 production (69.2% suppression), toll-like receptor (TLR) 2 induction, and mitogen-activated protein kinase (MAPK) phosphorylation in HGECs stimulated by P. gingivalis. Inoculation of mice with GPA inhibited P. gingivalis-induced alveolar bone resorption (25.6% suppression) by suppressing IL-6 and TLR2 production in the serum and gingiva. GPA suppressed osteoclast differentiation of bone marrow cells induced by M-CSF and sRANKL in mice (56.7% suppression). GPA also suppressed the mRNA expression of OSCAR, NFATc1, c-Fos, cathepsin K, and DC-STAMP. In summary, GPA exerts an anti-inflammatory effect on periodontal tissue and may be effective in preventing periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of Geniposidic Acid on Porphyromonas gingivalis-Induced Periodontitis in Mice

et al. 2022

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“…We recently reported that TLR4 is mainly important for the recognition of Mfa1 by gingival fibroblasts [ 17 ]. Takahashi et al reported that TLR2 may be important for Mfa1 recognition by bronchial epithelial cells [ 18 ]. Our results suggested that TLR2, along with TLR4, may be important for the recognition of Mfa1 and FimA by osteoclast progenitor cells.…”

Section: Discussionmentioning

confidence: 99%

“…In particular, TLR2 is important for P. gingivalis to produce proinflammatory cytokines [ 15 , 16 ]. It has been suggested that TLR2 and TLR4 may be involved in the recognition of P. gingivalis fimbriae [ 17 , 18 ], but a consensus has not been reached so far.…”

Section: Introductionmentioning

confidence: 99%

Porphyromonas gingivalis Fimbriae Induce Osteoclastogenesis via Toll-like Receptors in RAW264 Cells

Suzuki

Kikuchi

Goto

et al. 2022

IJMS

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The effect of Mfa1 fimbriae of Porphyromonas gingivalis on the progression of bone resorption remains unclear, especially compared with another fimbriae, FimA. We investigated the effect of Mfa1 on osteoclastogenesis together with FimA. We also investigated the role of Toll-like receptors (TLRs) in Mfa1 recognition during osteoclast differentiation. Receptor activator of nuclear factor κβ ligand (RANKL)-prestimulated RAW264 cells were used to examine the effects of purified Mfa1 fimbriae. The number of osteoclasts was examined by tartrate-resistant acid phosphate (TRAP) staining, osteoclast activation was investigated by bone resorption assays, and gene expression of differentiation markers was examined by quantitative real-time PCR. Transfection of Tlr2 and Tlr4 siRNAs into RAW264 cells was also employed and their role in Mfa1 recognition was investigated. Mfa1 effectively induced the formation of TRAP-positive multinucleated cells and activated osteoclasts. Mfa1 also increased gene expression of Acp5, Mmp9, and Ctsk in RANKL-prestimulated RAW264 cells compared with the control. The osteoclastogenesis induced by Mfa1 was significantly decreased in cells transfected with Tlr2 or Tlr4 siRNAs compared with control siRNA. Our results revealed the role of Mfa1 fimbriae in osteoclastogenesis that may contribute to the partial elucidation of the mechanisms of periodontal disease progression and the development of new therapeutic strategies.

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“…The binding of FimA to CXCR4 induces CR3 activation via phosphatidylinositol-3 kinase (PI3K) and inhibits the antibacterial response in macrophages ( 82 ). Similar to FimA, Mfa1 induces the production of pro-inflammatory factors through the activation of TLRs ( 83 , 84 ). Mfa1 inhibits the autophagy of DCs through the DC-SIGN-TLR2 crosstalk pathway, evading intracellular killing and leading to long-term survival within DCs ( 85 ).…”

Section: Pathogenicity Of P Gingivalis and Pathoge...mentioning

confidence: 99%

Porphyromonas gingivalis regulates atherosclerosis through an immune pathway

Ruan

Guan²,

Qi³

et al. 2023

Front. Immunol.

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Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several inflammatory diseases, among which periodontitis has been shown to increase the risk of AS. Porphyromonas gingivalis (P. gingivalis), presenting in large numbers in subgingival plaque biofilms, is the “dominant flora” in periodontitis, and its multiple virulence factors are important in stimulating host immunity. Therefore, it is significant to elucidate the potential mechanism and association between P. gingivalis and AS to prevent and treat AS. By summarizing the existing studies, we found that P. gingivalis promotes the progression of AS through multiple immune pathways. P. gingivalis can escape host immune clearance and, in various forms, circulate with blood and lymph and colonize arterial vessel walls, directly inducing local inflammation in blood vessels. It also induces the production of systemic inflammatory mediators and autoimmune antibodies, disrupts the serum lipid profile, and thus promotes the progression of AS. In this paper, we summarize the recent evidence (including clinical studies and animal studies) on the correlation between P. gingivalis and AS, and describe the specific immune mechanisms by which P. gingivalis promotes AS progression from three aspects (immune escape, blood circulation, and lymphatic circulation), providing new insights into the prevention and treatment of AS by suppressing periodontal pathogenic bacteria.

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Porphyromonas gingivalis Mfa1 fimbria putatively binds to TLR2 and induces both IL-6 and IL-8 production in human bronchial epithelial cells

Cited by 10 publications

References 31 publications

Anti-Inflammatory Effects of Geniposidic Acid on Porphyromonas gingivalis-Induced Periodontitis in Mice

Anti-Inflammatory Effects of Geniposidic Acid on Porphyromonas gingivalis-Induced Periodontitis in Mice

Porphyromonas gingivalis Fimbriae Induce Osteoclastogenesis via Toll-like Receptors in RAW264 Cells

Porphyromonas gingivalis regulates atherosclerosis through an immune pathway

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