Immunohistochemical detection of <i>Mycoplasma salivarium</i> in oral lichen planus tissue

Mizuki, Harumi; Abe, Ryosuke; Kogi, Shintaro; Mikami, Taisei

doi:10.1111/jop.12568

Cited by 17 publications

(16 citation statements)

References 24 publications

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“…reported that Mycoplasma salivarium was detected in 58.5% of OLP tissues by immunohistochemistry using an antibody to M. salivarium . The bacteria were localized intracellularly in epithelial cells although intracellular or extracellular localization in the lamina propria was not clear . Several Mycoplasma species, including M. salivarium , were detected among the buccal mucosal microbiota analyzed by our group, although there was no difference in relative abundance between control and OLP groups.…”

Section: Association With Bacterial Infectionmentioning

confidence: 57%

The microbiology of oral lichen planus: Is microbial infection the cause of oral lichen planus?

Baek

Choi

2017

Molecular Oral Microbiology

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SummaryOral lichen planus (OLP) is a variant of lichen planus (LP), a common chronic mucocutaneous inflammatory disease. Cutaneous lesions of LP are self-limiting, but OLP lesions are non-remissive, alternating periods of exacerbation and quiescence, and only symptomatic treatments exist for OLP. The precise etiology and pathogenesis of OLP are hardly understood, which is a major obstacle to the development of new therapeutics for this disease. OLP is considered a T-cell-mediated inflammatory disease.Although various antigens have been considered, what actually triggers the inflammatory response of T cells is unknown. Suggested predisposing factors include genetic factors, stress, trauma, and infection. The aim of this review was to determine whether microbial infection can cause OLP. We first reviewed the association between OLP and microbial factors, including viral, fungal, and bacterial infections. In addition, each microbial factor associated with OLP was assessed by modified guidelines of Fredricks and Relman to determine whether it establishes a causal relationship. In conclusion, no microbial factor yet fulfills the guidelines to establish the causality of OLP. By focusing on the unclarified issues, however, the potential roles of microbial factors in the pathogenesis of OLP will be soon elucidated. K E Y W O R D Sbacteria, causality, fungi, oral lichen planus, viruses | INTRODUCTIONLichen planus (LP), first described by Erasmus Wilson in 1869, is a common chronic mucocutaneous inflammatory disease affecting the skin, nails, eyes, urogenital tract, and oral mucosa.1 The prevalence of LP in the general population is 0.22%-5%. Although OLP is sometimes regarded as an autoimmune disorder, it is not classified as an autoimmune disease because no autoantigens have been identified. Suggested predisposing factors include genetic factors, stress, trauma, and infection. 5,6 In this article, microbial factors

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Section: Association With Bacterial Infectionmentioning

confidence: 57%

The microbiology of oral lichen planus: Is microbial infection the cause of oral lichen planus?

Baek

Choi

2017

Molecular Oral Microbiology

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“…S2). M. salivarium, the species detected in 58.5% of OLP tissues from Japanese patients 10 , was found in three OM samples at <0.1% but in none of the OT samples.…”

Section: Resultsmentioning

confidence: 89%

Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

Baek

Lee

et al. 2020

Sci Rep

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Oral lichen planus (OLP) is a chronic T cell-mediated inflammatory disease of unknown etiology. We previously proposed that the intracellular bacteria detected in oLp lesions are important triggering factors for T cell infiltration. This study aimed to identify OLP-associated bacterial species through the characterization of intratissue bacterial communities of OLP lesions. Seven pairs of bacterial communities collected from the mucosal surface and biopsied tissues of oLp lesions were analyzed by high-throughput sequencing of the 16S rRNA gene. The intratissue bacterial communities were characterized by decreased alpha diversity but increased beta diversity compared with those on the mucosal surface. While the relative abundance of most taxa was decreased within the tissues, that of Escherichia coli was significantly increased. Four E. coli strains were isolated from additional OLP biopsies and verified as K12 strains by whole-genome sequencing. The distribution of E. coli in sections of control (n = 12) and OLP (n = 22) tissues was examined by in situ hybridization. E. coli was detected in most OLP tissues, suggesting its potential role in the pathogenesis of OLP. The oral E. coli strains isolated from oLp tissues will be useful to investigate their role as triggering factors for t cell infiltration. Oral lichen planus (OLP) is a T cell-mediated chronic mucocutaneous disease of unknown etiology and is currently incurable. OLP occurs in 0.5-4% of the global population and appears more prevalent in females than males at a ratio of 1.5:1 1-3. The main histological features of OLP include band-like lymphocytic infiltration at the superficial part of connective tissue, the presence of liquefaction degeneration in the basal cell layer and the absence of epithelial dysplasia 4. Although the etiology and pathogenesis of OLP are not completely understood, unknown antigens are thought to trigger T cell infiltration and inflammatory responses of infiltrated lymphocytes such as CD4 + and CD8 + T cells 5. What triggers the activation and recruitment of T cells is an important question to find new therapeutics for OLP. Recently, many researchers have attempted to understand the relationship between human diseases and the human microbiome through high-throughput sequencing technology. To date, four research groups have studied the oral microbiota associated with OLP by sequencing the 16S rRNA gene, and differences in the microbiota of saliva and buccal mucosa between healthy controls and OLP patients have been reported 2,6-9. We previously reported increased bacterial invasion into the lamina propria, the presence of bacteria within basal epithelial cells and T cells in OLP lesions, and the induction of T cell chemokines by oral bacteria 6. In addition, Mizuki et al. reported that Mycoplasma salivarium was detected by immunohistochemistry in the epithelium and lymphocyte infiltrate area in 58.5% of OLP tissues from Japanese patients 10. These results suggest that oral bacteria may have a role in the pathogenesis of OLP. Howeve...

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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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Immunohistochemical detection of Mycoplasma salivarium in oral lichen planus tissue

Cited by 17 publications

References 24 publications

The microbiology of oral lichen planus: Is microbial infection the cause of oral lichen planus?

The microbiology of oral lichen planus: Is microbial infection the cause of oral lichen planus?

Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

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

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