Differential expression of Toll‐like receptor 4 in healthy and diseased human gingiva

Li, J.-P.; Chen, Y.; Ng, Corrie H. C.; Fung, Man-Lung; Xu, Aimin; Cheng, Bin; Tsao, Sai Wah; Leung, W. Keung

doi:10.1111/jre.12173

Cited by 20 publications

(29 citation statements)

References 21 publications

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“…The presence of TLR2-expressing inflammatory cells described in PG and PC indicated that the disease is likely to be sustained by the immune system via reactions to bacterial antigens. 5 , 9 , 10 The same conclusions have been drawn in the only TLR4 study, 9 where TLR4 has been found to be constitutive and non-constitutively expressed in human epithelial cells; 13 , 20 , 21 , 23 , 29 , 30 no data are available about its expression in ERM and the epithelium cyst lining of PC. The present study examined its expression in PL by immunohistochemistry focusing on the epithelial compartment.…”

Section: Discussionsupporting

confidence: 56%

Toll-like receptor 4 expression in the epithelium of inflammatory periapical lesions. An immunohistochemical study

et al. 2015

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Toll-like receptors (TLR) are essential for the innate immune response against invading pathogens and have been described in immunocompetent cells of areas affected by periapical disease. Besides initiating the inflammatory response, they also directly regulate epithelial cell proliferation and survival in a variety of settings. This study evaluates the in situ expression of TLR4 in periapical granulomas (PG) and radicular cysts, focusing on the epithelial compartment.Twenty-one periapical cysts (PC) and 10 PG were analyzed; 7 dentigerous non-inflamed follicular cyst (DC) served as control. TLR4 expression was assessed by immunohistochemistry. TLR4 immunoreaction products were detected in the epithelium of all specimens, with a higher percentage of immunostained cells in PG. Although TLR4 overexpression was detected in both PG and PC, there were differences that seemed to be related to the nature of the lesion, since in PG all epithelial cells of strands, islands and trabeculae were strongly immunoreactive for TLR4, whereas in PC only some areas of the basal and suprabasal epithelial layers were immunostained. This staining pattern is consistent with the action of TLR4: in PG it could promote formation of epithelial cell rests of Malassez and in epithelial strands and islands the enhancement of cell survival, proliferation and migration, whereas in PC TLR4 could protect the lining epithelium from extensive apoptosis. These findings go some way towards answering the intriguing question of why many epithelial strands or islands in PG and the lining epithelium of apical cysts regress after non-surgical endodontic therapy, and suggest that TLR4 plays a key role in the pathobiology of the inflammatory process related to periapical disease.

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Section: Discussionsupporting

confidence: 56%

Toll-like receptor 4 expression in the epithelium of inflammatory periapical lesions. An immunohistochemical study

et al. 2015

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“…However, this question is investigated rather poorly to date. TLR2 and TLR4 agonists are of especial interest in our study, because these receptors play a key role in the progression of periodontal disease 24 , 25 and are activated by bacterial components such as lipopolysaccharide, peptidoglycan, lipoteichoic acid, bacterial lipoproteins. Therefore, in the present study we investigated the simultaneous effect of IFN-γ and TLR2 and TLR4 agonists on the expression of immunomodulatory protein IDO-1 and inflammatory mediators interleukin (IL) 6, IL-8, and MCP-1 in hPDLCS.…”

Section: Introductionmentioning

confidence: 99%

Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists

Andrukhov

Hong

Andrukhova

et al. 2017

Sci Rep

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Periodontal ligament stem cells similarly to the mesenchymal stem cells of other tissues possess immunomodulatory properties, which are regulated by different cytokines, particularly by interferon-γ (IFN-γ). In contrast, less information is provided about the effect of toll-like receptors ligand on immunomodulatory properties of these cells. In the present study we investigated the response of human periodontal ligament stem cells (hPDLSCs) in response to simultaneous stimulation with IFN-γ and toll-like receptor (TLR) agonists. The resulting expression of indoleamine-2,3-dioxygenase-1 (IDO-1), interleukin (IL)-6, IL-8 and monocyte chemotactic protein 1 (MCP-1) was investigated. The expression of IDO-1 was upregulated by IFN-γ in both gene and protein levels. TLR2 agonist Pam3CSK4 induced gene expression of IDO-1, but had no effect on protein expression. IFN-γ induced IDO-1 protein expression was further enhanced by Pam3CSK4. TLR-4 agonist E. coli LPS has no significant effect on neither basal nor IFN-γ induced IDO-1 protein expression. The production of IL-6, IL-8, and MCP-1 was induced by TLR agonists. Neither basal nor TLR agonists induced production of these proteins was affected by IFN-γ. Our data shows potential interaction between IFN-γ and TLR2 responses in hPDLSCs, which might be involved in regulation of immune response in inflammatory diseases, and particularly periodontitis.

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“…The accumulation of HIF-1α may be modulated by TLRs and patern recognition in certain ways, since a TLR4 neutralizing antibody could atenuate such an efect from E. coli LPS. Moreover, the expression of TLR4, CD14, and MD-2 in both human gingival keratinocytes and ibroblasts is conirmed, and the TLR4 protein expression in periodontal epithelial compartments appeared diferent in vivo, indicating that LPS sensing in the dentogingival front in health could be heterogeneous in nature [92].…”

Section: Hif In the Periodontopathogen-host Cross Talkmentioning

confidence: 90%

Role of the Hypoxia-Inducible Factor in Periodontal Inflammation

Wang¹,

Chen²,

Leung³

2017

Hypoxia and Human Diseases

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Human periodontitis is a chronic inlammatory disease induced by opportunistic Gramnegative anaerobic bacteria at the tooth-supporting apparatus. Within the gingivitisafected sulcus or periodontal pocket, the resident anaerobic bacteria interact with the host inlammatory reactions leading to a lower oxygen or hypoxic environment. A cellular/tissue oxygen-sensing mechanism and its appropriate regulation are needed to assist tissue adaptation to natural/pathology-induced variations in oxygen availability. In this chapter, we reviewed the biological relevance of hypoxia in periodontal/oral cellular development, epithelial barrier function, periodontal inlammation, and immunity. The role of hypoxia-inducible factor-1α in pathogen-host cross talk and alveolar bone homeostasis was also discussed. The naturally occurring pathophysiological process of hypoxia appeared to entail fundamental relevance for periodontal defense and regeneration.

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Differential expression of Toll‐like receptor 4 in healthy and diseased human gingiva

Abstract: TLR4, CD14 and MD-2, but not LBP, are expressed in human gingival keratinocytes and fibroblasts. The TLR4 expression level in the junctional epithelium appeared to be lowest within the periodontal epithelial barrier.

Cited by 20 publications

References 21 publications

Toll-like receptor 4 expression in the epithelium of inflammatory periapical lesions. An immunohistochemical study

Toll-like receptor 4 expression in the epithelium of inflammatory periapical lesions. An immunohistochemical study

Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists

Role of the Hypoxia-Inducible Factor in Periodontal Inflammation

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