<i>Porphyromonas gingivalis</i> lipopolysaccharide induces over production of <scp>CC</scp> chemokine ligand 2 via toll‐like receptor‐4 in oral lichen planus

Zeng, Qi; Yang, Xi; Chen, Xiaobing; Xia, Juan; Cheng, Bin; Tao, Xiaoan

doi:10.1111/jop.12655

Cited by 12 publications

(13 citation statements)

References 27 publications

(36 reference statements)

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“…Recently, several studies have suggested that microorganisms may trigger or be responsible for sustaining or exacerbating the chronic course of OLP [ 32 – 34 ]. Epithelial barrier dysfunction may precede intracellular infection of basal epithelial cells with bacteria, virus, or possibly fungus.…”

Section: Discussionmentioning

confidence: 99%

Oral lichen-planus-associated fibroblasts acquire myofibroblast characteristics and secrete pro-inflammatory cytokines in response to Porphyromonas gingivalis lipopolysaccharide stimulation

et al. 2018

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BackgroundOral lichen planus (OLP) is a chronic inflammatory oral mucosal disease in which comprehensive inflammation-related cytokines are involved. These cytokines are commonly produced by immune cells and specific nonimmune cells including keratinocytes, endothelial cells and fibroblasts. This raises the question of whether fibroblasts in OLP lesions contribute to the inflammatory process upon inflammatory simulation.MethodsPrimary cultured Oral lichen-planus-associated fibroblasts (OLP AFs, n = 5) and normal buccal mucosal fibroblasts (NFs, n = 5) were examined by immunohistochemistry, Western blotting and reverse transcription-polymerase chain reactions (RT-PCR). Various inflammatory mediators were evaluated with a multiplex assay. Differences among groups were assessed using a Student’s test or repeated measures one-way ANOVA, as appropriate.ResultsOLP AFs express significantly higher levels of α-smooth muscle actin (α-SMA) than NFs, indicating the presence of myofibroblasts. Myofibroblasts secrete Interleukin (IL)-6, IL-8, and tumor necrosis factor-α (TNF-α) in response to Porphyromonas gingivalis lipopolysaccharide (pg. LPS).ConclusionOLP AFs demonstrated α-SMA expression and secreted pro-inflammatory cytokines in response to pg. LPS stimulation.Electronic supplementary materialThe online version of this article (10.1186/s12903-018-0656-6) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Oral lichen-planus-associated fibroblasts acquire myofibroblast characteristics and secrete pro-inflammatory cytokines in response to Porphyromonas gingivalis lipopolysaccharide stimulation

et al. 2018

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“…According to literature, the pathogenesis of OLP is associated with dysregulated T-cell responses to exogenous triggers and an antigen-specific mechanism by keratinocytes and Langerhans cells resulting in the activation of T-cells [ 110 ]. It has been observed that the normal buccal fibroblasts secreted weaker cytokines than the OLP associated fibroblast under LPS stimulation [ 110 , 111 , 112 ].…”

Section: Systemic Effects Related To Endotoxins Secreted By Microorganisms Involved In Periodontitismentioning

confidence: 99%

Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease

Marcano

Córdoba-Díaz

et al. 2021

Toxins

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It is widely recognized that periodontal disease is an inflammatory entity of infectious origin, in which the immune activation of the host leads to the destruction of the supporting tissues of the tooth. Periodontal pathogenic bacteria like Porphyromonas gingivalis, that belongs to the complex net of oral microflora, exhibits a toxicogenic potential by releasing endotoxins, which are the lipopolysaccharide component (LPS) available in the outer cell wall of Gram-negative bacteria. Endotoxins are released into the tissues causing damage after the cell is lysed. There are three well-defined regions in the LPS: one of them, the lipid A, has a lipidic nature, and the other two, the Core and the O-antigen, have a glycosidic nature, all of them with independent and synergistic functions. Lipid A is the “bioactive center” of LPS, responsible for its toxicity, and shows great variability along bacteria. In general, endotoxins have specific receptors at the cells, causing a wide immunoinflammatory response by inducing the release of pro-inflammatory cytokines and the production of matrix metalloproteinases. This response is not coordinated, favoring the dissemination of LPS through blood vessels, as well as binding mainly to Toll-like receptor 4 (TLR4) expressed in the host cells, leading to the destruction of the tissues and the detrimental effect in some systemic pathologies. Lipid A can also act as a TLRs antagonist eliciting immune deregulation. Although bacterial endotoxins have been extensively studied clinically and in a laboratory, their effects on the oral cavity and particularly on periodontium deserve special attention since they affect the connective tissue that supports the tooth, and can be linked to advanced medical conditions. This review addresses the distribution of endotoxins associated with periodontal pathogenic bacteria and its relationship with systemic diseases, as well as the effect of some therapeutic alternatives.

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“…Moreover, LPS is the main component of bacterial cell walls and is an endotoxin that can elicit a strong immune response. Although there is no direct evidence to establish the causality of OLP and microbial factors, oral bacteria had been proved to participate in the pathogenesis of OLP via the TLR‐4 pathway (Zeng et al, ). In our study, we have confirmed the levels of TNF‐α and IL‐6 were higher in OLP tissues compared to healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Role of mammary serine protease inhibitor on the inflammatory response in oral lichen planus

Liu

et al. 2019

Oral Diseases

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Objectives Oral lichen planus (OLP) is a chronic inflammatory condition with an unclear pathological mechanism. IκB kinase α (IKKα)‐regulated mammary serine protease inhibitor (MASPIN) has been shown to mediate inflammation, particularly in cancers. Here, we explored the expression of MASPIN in OLP and its role in the inflammatory response. Materials and Methods Immunohistochemistry staining and reverse transcription‐polymerase chain reaction assays were used to detect the subcellular localization and expression of MASPIN and IKKα in OLP and healthy control tissues. Levels of the inflammatory factors were compared with enzyme‐linked immunosorbent assays. MASPIN and IKKα were overexpressed and silenced, respectively, in an inflammation model of human oral keratinocytes (HOKs) stimulated with lipopolysaccharide (LPS). Results Mammary serine protease inhibitor expression was down‐regulated, whereas IKKα expression was up‐regulated in OLP tissues (p < 0.01). The levels of tumour necrosis factor‐alpha and interleukin‐6 in OLP tissues were increased compared to those of healthy controls (p < 0.01). MASPIN overexpression in LPS‐stimulated HOK cells inhibited the levels of IKKα and the secretion of inflammatory cytokines. By contrast, IKKα silencing promoted the expression of MASPIN and inhibited the secretion of inflammatory cytokines. Conclusion Both MASPIN and IKKα are involved in the inflammatory process of OLP, suggesting potential therapeutic targets.

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Porphyromonas gingivalis lipopolysaccharide induces over production of CC chemokine ligand 2 via toll‐like receptor‐4 in oral lichen planus

Abstract: Increased TLR-4 expression contributes to the upregulated expression of CCL2 in the epithelium of OLP lesions, which suggests that oral bacteria participate in the pathogenesis of OLP via the TLR-4 pathway.

Cited by 12 publications

References 27 publications

Oral lichen-planus-associated fibroblasts acquire myofibroblast characteristics and secrete pro-inflammatory cytokines in response to Porphyromonas gingivalis lipopolysaccharide stimulation

Oral lichen-planus-associated fibroblasts acquire myofibroblast characteristics and secrete pro-inflammatory cytokines in response to Porphyromonas gingivalis lipopolysaccharide stimulation

Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease

Role of mammary serine protease inhibitor on the inflammatory response in oral lichen planus

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