Adhesion of monocytes to periodontal fibroblasts requires activation of NOD1/2- and TLR4-mediated LFA-1 and VLA-4

Liu, Jianru; Liu, Wenyi; Xie, Ying; Wang, Yixiang; Ouyang, Xiangying

doi:10.1016/j.archoralbio.2014.12.012

Cited by 5 publications

(7 citation statements)

References 35 publications

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“…Healthy and diseased human gingival tissues are shown to express high levels of NOD1 and NOD2 in epithelial cells and inflammatory cells, with no difference reported among different periodontal conditions. [60][61][62] In a preclinical study Nod2 −/− and Rip2 −/− (downstream kinase of Nod1 and Nod2) mice showed a significant reduction of experimental alveolar bone resorption and osteoclastogenesis, supporting NOD2 as a driver of periodontal bone loss. 63 This result is contradictory to the findings of a collaborative effort developed by the authors in which Nod2 −/− mice showed no difference in the amount of bone loss compared with controls.…”

Section: Nod1 and Nod2mentioning

confidence: 97%

“…There is a paucity of information regarding the relevance of NOD1 and NOD2 in periodontitis. Healthy and diseased human gingival tissues are shown to express high levels of NOD1 and NOD2 in epithelial cells and inflammatory cells, with no difference reported among different periodontal conditions . In a preclinical study Nod2 −/− and Rip2 −/− (downstream kinase of Nod1 and Nod2) mice showed a significant reduction of experimental alveolar bone resorption and osteoclastogenesis, supporting NOD2 as a driver of periodontal bone loss .…”

Section: Inflammasomes and Disease Pathogenesismentioning

confidence: 99%

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Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics

Marchesan

Girnary

Moss

et al. 2019

Periodontology 2000

106

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Inflammasomes are a group of multimolecular intracellular complexes assembled around several innate immune proteins. Recognition of a diverse range of microbial, stress and damage signals by inflammasomes results in direct activation of caspase‐1, which subsequently induces the only known form of secretion of active interleukin‐1β and interleukin‐18. Although the importance of interleukin‐1β in the periodontium is not questioned, the impact of inflammasomes in periodontal disease and its potential for therapeutics in periodontology is still in its very early stages. Increasing evidence in preclinical models and human data strongly implicate the involvement of inflammasomes in a number of inflammatory, autoinflammatory and autoimmune disorders. Here we review: (a) the currently known inflammasome functions, (b) clinical/preclinical data supporting inflammasome involvement in the context of periodontal and comorbid diseases and (c) potential therapies targeting inflammasomes. To clarify further the inflammasome involvement in periodontitis, we present analyses of data from a large clinical study (n = 5809) that measured the gingival crevicular fluid‐interleukin‐1β and grouped the participants based on current periodontal disease classifications. We review data on 4910 European‐Americans that correlate 16 polymorphisms in the interleukin‐1B region with high gingival crevicular fluid‐interleukin‐1β levels. We show that inflammasome components are increased in diseased periodontal tissues and that the caspase‐1 inhibitor, VX‐765, inhibits ~50% of alveolar bone loss in experimental periodontitis. The literature review further supports that although patients clinically present with the same phenotype, the disease that develops probably has different underlying biological pathways. The current data indicate that inflammasomes have a role in periodontal disease pathogenesis. Understanding the contribution of different inflammasomes to disease development and distinct patient susceptibility will probably translate into improved, personalized therapies.

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Section: Nod1 and Nod2mentioning

confidence: 97%

Section: Inflammasomes and Disease Pathogenesismentioning

confidence: 99%

Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics

Marchesan

Girnary

Moss

et al. 2019

Periodontology 2000

106

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“…As shown in Figure 8A,B well as their counterligands. 18,41 In the present study, VCAM-1 expression of HGFs seems to be upregulated by PM exposure, which then functions as a crucial factor aiding the adhesion of monocytic cells, eventually contributing to the inflammatory progression. To the best of our knowledge, this is the first evidence linking PM exposure with VCAM-1 expression and monocyte adhesion in HGFs thus far.…”

Section: Surfactin Inhibits Pm-induced Il-6 and Vcam-1 Expression In Mouse Gingival Tissuesmentioning

confidence: 48%

Surfactin reduces particulate matter–induced VCAM‐1–dependent monocyte adhesion in human gingival fibroblasts by increasing Nrf2‐dependent HO‐1 expression

Huang

Wee

et al. 2021

J of Periodontal Research

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Background and objectives:The mechanisms of particulate matter (PM) toxicity involve the generation of ROS and upregulation of proinflammatory molecules. Nrf2 is a multifunctional cytoprotective transcription factor that regulates the expression of various antioxidant, anti-inflammatory, and detoxifying molecules, such as HO-1.As surfactin has potential to induce Nrf2 activation and HO-1 expression, this study aimed to investigate the anti-inflammatory effects of surfactin on PM-exposed human gingival fibroblasts (HGFs) and signaling pathways engaged by surfactin. Materials and methods: Human gingival fibroblasts were challenged by PM with or without surfactin pretreatment. The expression of Nrf2, HO-1, VCAM-1, and other molecules was determined by western blot, real-time PCR, or ELISA. Human monocytic THP-1 cells labeled with fluorescent reagent were added to HGFs, and the cell adhesion was assessed. ROS generation and NADPH oxidase activity were also measured. The involvement of Nrf2/HO-1 and ROS signaling pathways was investigated by treating HGFs with specific pathway interventions, genetically or pharmacologically.One dose of surfactin was given to mice before PM treatment to explore its in vivo effect on VCAM-1 expression in gingival tissues.

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“…Studies have also shown that CD14 ( [6,25], and this study) as well as TLR2 and TLR4 are expressed on human GFs and, thus, mediate pathogen interactions with GFs. Liu et al (2015) exposed a monocytic cell line to a TLR4 agonist, which enhanced the expression of adherence genes LFA-1 and VLA-4, suggesting that binding of monocytes to fibroblasts is likely partly regulated by LFA-1 and VLA-4 [26,27].…”

Section: The Role Of Monocytes In Tlr Activationmentioning

confidence: 99%

T Cell Proliferation Is Induced by Chronically TLR2-Stimulated Gingival Fibroblasts or Monocytes

Moonen

Karlis

Schoenmaker

et al. 2019

IJMS

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During inflammation of the gums, resident cells of the periodontium, gingival fibroblasts (GFs), interact with heterogeneous cell populations of the innate and adaptive immune system that play a crucial role in protecting the host from pathogenic infectious agents. We investigated the effects of chronic inflammation, by exposing peripheral blood mononuclear cells (PBMCs), peripheral blood lymphocyte (PBL) cultures, and GF–PBMC cocultures to Toll-like receptor 2 (TLR2) and TLR4 activators for 21 days and assessed whether this influenced leukocyte retention, survival, and proliferation. Chronic stimulation of PBMC–GF cocultures with TLR2 and TLR4 agonists induced a reduction of NK (CD56+CD3−), T (CD3+), and B (CD19+) cells, whereas the number of TLR-expressing monocytes were unaffected. TLR2 agonists doubled the T cell proliferation, likely of a selective population, given the net decrease of T cells. Subsequent chronic exposure experiments without GF, using PBMC and PBL cultures, showed a significantly (p < 0.0001) increased proinflammatory cytokine production of TNF-α and IL-1β up to 21 days only in TLR2-activated PBMC with concomitant T cell proliferation, suggesting a role for monocytes. In conclusion, chronic TLR activation mediates the shift in cell populations during infection. Particularly, TLR2 activators play an important role in T cell proliferation and proinflammatory cytokine production by monocytes, suggesting that TLR2 activation represents a bridge between innate and adaptive immunity.

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Adhesion of monocytes to periodontal fibroblasts requires activation of NOD1/2- and TLR4-mediated LFA-1 and VLA-4

Cited by 5 publications

References 35 publications

Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics

Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics

Surfactin reduces particulate matter–induced VCAM‐1–dependent monocyte adhesion in human gingival fibroblasts by increasing Nrf2‐dependent HO‐1 expression

T Cell Proliferation Is Induced by Chronically TLR2-Stimulated Gingival Fibroblasts or Monocytes

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