Human periodontal ligament cells facilitate leukocyte recruitment and are influenced in their immunomodulatory function by Th17 cytokine release

Konermann, Anna; Beyer, Marc; Deschner, James; Allam, Jean‐Pierre; Novak, Natalija; Winter, Jochen; Jepsen, Søren; Jäger, Andreas

doi:10.1016/j.cellimm.2011.10.020

Cited by 36 publications

(28 citation statements)

References 42 publications

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“…22 The recruitment of mononuclear cells can be observed during the resorption process. [19][20][21]28 Odontoclasts are needed for the resorption of the mineralized matrix of dental tissues. Odontoclasts are the same cell type as osteoclasts, and they are both called clastic cells.…”

Section: Discussionmentioning

confidence: 99%

“…PDL cells were cultured as described previously. 28 Briefly, the PDL was gently scraped off from the middle third of the root surface to avoid contamination from the gingival and apical tissues. The tissue explants were transferred to cell culture flasks containing Dulbecco's Modified Eagle's Medium (DMEM; Gibco â BRL, Thermo Fisher Scientific, Waltham, MA, USA) supplemented with antibiotics (penicillin 100 U/mL, streptomycin 100 lg/ mL) and 10% fetal bovine serum (FBS; Gibco â BRL, Thermo Fisher Scientific, Waltham, MA, USA).…”

Section: Cell Culturementioning

confidence: 99%

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Upregulated expression of monocyte chemoattractant protein‐1 in human periodontal ligament cells induced by interleukin‐1β

Jin

Cao

2015

Australian Dental Journal

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Background: Root resorption during orthodontic treatment is a complex and sterile inflammatory process, characterized by the recruitment of mononuclear cells in the local periodontal ligament. This study aimed to investigate whether interleukin (IL)-1b could induce the migration of monocytes through upregulating monocyte chemoattractant protein (MCP)-1 expression in human periodontal ligament cells. Methods: Human periodontal ligament cells were cultured in medium containing various IL-1b concentrations. After 24 hours of incubation, the messenger RNA (mRNA) and MCP-1 protein in periodontal ligament cells were detected by reverse transcriptase-polymerase chain reaction and Western blot analysis, respectively. The effect of supernatants of periodontal ligament cells on THP-1 cells was analysed via migration assay. Results: IL-1b (10 ng/mL and 25 ng/mL) increased the expression of MCP-1 mRNA and protein in periodontal ligament cells (p < 0.05). In addition, the supernatants from the IL-1b-treated periodontal ligament cells increased the migratory response of THP-1 cells (p < 0.05), which could be blocked by the anti-MCP-1 antibody. Conclusions: IL-1b had the potential to induce the migratory response of monocytes via upregulation of the expression of MCP-1 in human periodontal ligament cells and could contribute to orthodontic root resorption.

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Section: Discussionmentioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

Upregulated expression of monocyte chemoattractant protein‐1 in human periodontal ligament cells induced by interleukin‐1β

Jin

Cao

2015

Australian Dental Journal

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“…Th17 cells also produce IL-6, IL-1β, TNF-α, IL-21, IL-22, IL-23, IL-26 and Receptor Activator of Nuclear factor Kappa B Ligand (RANKL) Hajishengallis, 2014). The expansion of human Th17 cells is regulated by IL-23, whereas IL-1, TGF-β1 and IL-6 initiate the differentiation of Th17 (Konermann et al, 2012). Moreover, IL-21, as an autocrine-regulating factor for Th17 cells, plays an important role in inducing the differentiation of Th17 cells and inhibition of Th1 and Treg function (Zhao et al, 2011).…”

Section: The Microbial Challenge: Cellular and Molecular Mechanisms Imentioning

confidence: 99%

“…It has been suggested a possible role for periodontal ligament fibroblasts by upregulating the chemotactic MIP-3α that attract Th17 cells into the inflamed periodontal tissues (Konermann et al, 2012), where these lymphocytes mediate tissue damage. Th17 lymphocyte may provide protection because they attract neutrophils and induce the expression of antimicrobial factors.…”

Section: The Microbial Challenge: Cellular and Molecular Mechanisms Imentioning

confidence: 99%

“…Th17 lymphocyte may provide protection because they attract neutrophils and induce the expression of antimicrobial factors. However, they may also contribute to pathogenesis of autoimmune inflammatory disease, by causing osteoclastogenesis (IL-17 and RANKL) (Konermann et al, 2012). Th17 cells are observed at sites with CP and related Th17 cytokines are produced in periodontal lesions Hajishengallis, 2014).…”

Section: The Microbial Challenge: Cellular and Molecular Mechanisms Imentioning

confidence: 99%

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Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms

Leite¹,

Carneiro²,

Nunes

et al. 2015

American Journal of Immunology

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Periodontal Diseases (PD) are characterized by pathological manifestation of host immune response to bacterial infection at the tooth/gingival interface. Evidences points periodontitis as a risk factor for pathological systemic conditions, such as, cardiovascular diseases and diabetes. The identification of host factors that determine their susceptibility to immune subversion can provide useful information in the pathogenesis of periodontitis. Protective acute inflammatory response fails to remove inflammatory cells, especially neutrophils, evolving to chronic, destructive and pathological lesions. T and B cells actively participate in pathogenesis of the disease. CD4+ naive T cells are activated by antigenic stimulation and differentiate into subpopulations of distinct effector cells, characterized by its specific cytokine production profiles and functions. In periodontal infection, activated Th17 and regulatory T lymphocytes (Tregs) play antagonistic roles as effector and suppressor cells, respectively. In presence of Tregs, there is a decrease in the levels of pro-inflammatory cytokines, such as, Interferon gamma (IFN-γ), Interleukin (IL) -17, Tumor Necrosis Factor (TNF) and IL-1 β, at sites of disease. Absence of Tregs may cause a variety of disorders, such as, periodontitis. The RANKL/RANK system and Osteoprotegerin (OPG) are modulators of bone resorption in periodontitis. The balance between periodontal bone resorption by osteoclasts and bone formation by osteoblasts controls bone mass. RANKL induces osteoclast differentiation and maturation and OPG inhibits RANK/RANKL interaction and prevents bone resorption. RANKL mRNA and the RANKL/OPG mRNA ratio were enhanced in chronic periodontitis. Furthermore, the role of NF-kB, FoxP3 and T-bet transcription factors were explored. Therapies for periodontitis involving cellular and molecular biology are not specific and have many side effects. Current therapies to successfully control the PD reduces clinical signs of inflammation at local sites of the disease; however, new treatments for periodontitis should address the contribution of immune cells in bone resorption, particularly in the natural course of the disease, considering its periods of remission and progression.

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Immunomodulation by adult stem cells

Davies

Blanc

2016

Tissue Engineering and Regeneration in Dentistry

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Human periodontal ligament cells facilitate leukocyte recruitment and are influenced in their immunomodulatory function by Th17 cytokine release

Cited by 36 publications

References 42 publications

Upregulated expression of monocyte chemoattractant protein‐1 in human periodontal ligament cells induced by interleukin‐1β

Upregulated expression of monocyte chemoattractant protein‐1 in human periodontal ligament cells induced by interleukin‐1β

Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms

Immunomodulation by adult stem cells

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