Hypha essential genes in Candida albicans pathogenesis of oral lichen planus: an in-vitro study.

BACKGROUND: Hypha essential genes (HEGs) of Candida Albicans have been emerging into scholar's attention, little known about their functions in oral lichen planus (OLP) with an uncovered etiology. This research aimed to observe necessary genes in biphasic C. albicans from OLP and study their relevance in pathogenesis, so as to evaluate possible roles of morphologic switching in etiology of OLP. METHODS: Samples were collected from OLP lesions of patients, mycelia were cultured and total RNA was extracted then subjected to reverse transcription-PCR and real-time PCR. RESULTS: HWP1 and HGC1 were significantly expressed in hyphae phase and weakly detected in yeast phase, while there was no significant difference of EFG1, ALS3, and ECE1 between in yeast and mycelia. CONCLUSION: HGC1 and HWP1 were confirmed to be hypha essential genes, with HGC1 for hypha morphogenesis and HWP1 for adhesion invasion in pathogenesis of C. albicans in OLP. ALS3, ECE1 and EFG1 played minor roles in hyphae maintenance and adhesion for hyphae. These might be deemed as hints for the etiology of OLP and indicate HGC1 and HWP1 to be a priority of potential drug target.

Helicobacter pylori infection is correlated with the incidence of erosive oral lichen planus and the alteration of the oral microbiome composition.

BACKGROUND: Oral lichen planus (OLP), a common clinical oral disease, is associated with an increased risk of malignant transformation. The mechanism underlying the pathogenesis of OLP is unknown. Oral dysbacteriosis is reported to be one of the aetiological factors of OLP. Although Helicobacter pylori infection is associated with various oral diseases, the correlation between H. pylori infection and OLP is unclear. This study aimed to investigate the effect of H. pylori infection on OLP pathogenesis and oral microbiome composition in the Chinese population, which has a high incidence of H. pylori infection. RESULT: In this study, saliva samples of 30 patients with OLP (OLP group) and 21 negative controls (NC group) were collected. H. pylori infection was detected using the carbon-13-labeled urea breath test (UBT). The saliva samples were divided into the following four groups based on the H. pylori status: H. pylori-positive OLP (OLP+), H. pylori-positive NC (NC+), H. pylori-negative OLP (OLP-), and H. pylori-negative NC (NC-). Oral microbiome compositions were significantly different between the OLP and NC groups and between the OLP- and OLP+ groups. Compared with those in the OLP- group, those in the OLP+ group had a higher incidence of erosive OLP and higher levels of salivary cytokines. In contrast, the oral microbiome composition and cytokine levels were not significantly different between the NC- and NC+ groups. CONCLUSIONS: This is the first report to demonstrate that H. pylori infection is significantly correlated with the pathogenesis of erosive OLP.

Oral lichen planus: a microbiologist point of view.

Oral lichen planus (OLP) is a chronic disease of uncertain etiology, although it is generally considered as an immune-mediated disease that affects the mucous membranes and even the skin and nails. Over the years, this disease was attributed to a variety of causes, including different types of microorganisms. This review analyzes the present state of the art of the disease, from a microbiological point of view, while considering whether or not the possibility of a microbial origin for the disease can be supported. From the evidence presented here, OLP should be considered an immunological disease, as it was initially proposed, as opposed to an illness of microbiological origin. The different microorganisms so far described as putative disease-causing agents do not fulfill Koch's postulates; they are, actually, not the cause, but a result of the disease that provides the right circumstances for microbial colonization. This means that, at this stage, and unless new data becomes available, no microorganism can be envisaged as the causative agent of lichen planus.

Omega-3 polyunsaturated fatty acids: a promising approach for the management of oral lichen planus.

BACKGROUND: Oral lichen planus (OLP) is a T-cell-mediated inflammatory disease with a risk of malignant transformation. Although the etiology of OLP is still uncertain, growing evidence suggests that oral microbiota, antigen-specific, and non-specific mechanisms are involved in the pathogenesis of OLP. Antigen-specific mechanisms include antigen presentation, T-cell activation, nuclear factor-kappa B signaling pathway, and cytokine secretion, while non-specific mechanisms consist of matrix metalloproteinases (MMP)-9 upregulation, psychological pressure, oxidative damage, aberrant expression of microRNAs (miRNAs), and autophagy. Till now, there is no cure for OLP, and the main purpose of OLP therapy is symptomatic control. FINDING: Seafood and its derivative omega-3 polyunsaturated fatty acids (n-3 PUFAs) can suppress antigen presentation, T-cell activation, and nuclear factor-kappa B signaling pathway, modulate the overexpressed inflammatory cytokines, inhibit the expression of MMP-9, as well as regulate the expression of miRNAs and autophagy. And they are possible agents for ameliorating psychological disorder and oxidative damage. Moreover, n-3 PUFAs supplementation has a beneficial effect on preventing tumorigenesis. CONCLUSION: n-3 PUFAs consumption may provide a non-toxic, inexpensive administration for OLP.

Dysbiosis of saliva microbiome in patients with oral lichen planus.

BACKGROUND: Oral microbiota is not only important for maintaining oral health but also plays a role in various oral diseases. However, studies regarding microbiome changes in oral lichen planus (OLP) are very limited. To the best of our knowledge, there has been only two studies investigating salivary microbiome changes in OLP. Therefore, the purpose of this study was to identify the characteristic microbial profile in the saliva of OLP patients, with or without erosive lesions, and compare that with recurrent aphthous ulcer (RAU), a common oral immunological disorder that also shows multiple erosive/ulcerative lesions. Whole saliva samples were collected from 20 patients with OLP (erosive E, n = 10 and non-erosive NE, n = 10), 10 patients with RAU (U) and 10 healthy controls (C). DNA was extracted from the saliva samples, and the 16S rDNA gene V4 hypervariable region was analyzed using Illumina sequencing. RESULTS: We obtained 4949 operational taxonomic units (OTUs) from the V4 region in all saliva samples. Community composition analysis showed a clear decreased relative abundance of genera Streptococcus and Sphingomonas in saliva from RAU patients when compared to the other three groups. Relative abundance of Lautropia and Gemella were higher in E group, whereas relative abundance of Haemophilus and Neisseria were higher in NE group when compared to C group. Abiotrophia and Oribacterium were higher in OLP (combining E and NE groups), while Eikenella and Aggregatibacter were lower when compared to C group. There was statistically significance in α-diversity between E and RAU groups(p < 0.05). Significant differences in ß-diversity were detected in bacteria between E and C; NE and C; as well as E and NE groups. The LDA effect size algorithm identified the g_Haemophilus might be the potential biomarker in NE group. CONCLUSIONS: We found that salivary microbiome in erosive OLP was significantly different from that found in RAU; and these changes may be related to the underlying disease process rather than presence of ulcerative/erosive lesions clinically. In addition, our findings in bacterial relative abundance in OLP were significantly different from the previously reported findings, which points to the need for further research in salivary microbiome of OLP.

A pilot study: a possible implication of Candida as an etiologically endogenous pathogen for oral lichen planus.

BACKGROUND: The aim of this study was to investigate the prevalence and genotypic profiles of Candida albicans in patients with oral lichen planus (OLP). MATERIALS AND METHODS: Positive rates and genotypic profiles of Candida albicans strains from OLP patients and healthy controls were analyzed. Random amplified polymorphic DNA and internal transcribed spacer of ribosome DNA polymerase chain reactions were used to sequence the DNA of these strains, and then their genetic similarity was measured using BLAST, UIV Band, and Vector NTI Suite Sequence Analyses Software. RESULTS: The prevalence of C. albicans strains detected from erosive-OLP, non-erosive OLP, and normal individuals was 18.87, 18.75, and 7.92%, respectively. Four different genotypes were revealed by the two methods. To be specific, type I was found only in the healthy subjects; type II a and II b were found in non-erosive OLP, and type III was identified in erosive OLP. Intragroup similarity coefficients, i.e. SAB were 100%, and inter-groups similarity coefficients, i.e. SAB were less than 30%. CONCLUSIONS: The genotypic results of C. albicans in OLP revealed an endogenous rather than exogenous infection of C. albicans. In addition, a possible pathogenic role of C. albicans in OLP, with the etiologic sense contributing to a more proper recognition on the pathogenesis, development, and progression of OLP, as well as some strategies for its diagnosis and treatment were identified.

Probable Association Between Oral Lichen Planus and presence of Helicobacter Pylori: a Preliminary Study in a Chilean Population / Probable Asociación entre Liquen plano Oral y la presencia de Helicobacter pylori: estudio Preliminar en Chile

ABSTRACT: Oral Lichen planus (OLP) is one of the main inflammatory diseases of the oral mucosa that is considered as a potentially malignant disorder. The exact pathogenesis of OLP remains to be completely understood. However, presence of bacteria has been associated to the inflammatory response observed in OLP. Particularly, Helicobacter pylori a major etiological agent of gastrointestinal inflammatory diseases and risk factor for gastric cancer, has been associated to Lichen planus. Here we studied a group of Chilean patients if there is any association between the presence of Helicobacter pylori and the clinical manifestation of OLP. We found a significant difference between the patients positive for H. pylori and the age of OLP diagnosis, suggesting that oral H. pylori might induce the disease at an earlier age. However, we could not confirm a statistically significance between the presence of the bacteria and OLP.

RESUMEN: Liquen Plano Oral (LPO) es una enfermedad inflamatoria de la mucosa oral considerada como desorden potencialmente maligno. La patogénesis exacta de LPO es desconocida. Sin embargo, se ha asociado la presencia de bacterias como responsables de la inflamación observada en LPO. Particularmente, Helicobacter pylori (H. pylori), agente etiológico principal de enfermedades inflamatorias gastrointestinales y factor de riesgo de cáncer gástrico, ha sido asociado con LPO. Se estudió la posible asociación entre H. pylori y manifestaciones clínicas de LPO en un grupo de pacientes Chilenos. Se encontró diferencia significativa entre los pacientes positivos para H. pylori y la edad de diagnóstico de LPO, sugiriendo que H. pylori podría inducir la enfermedad a temprana edad. Sin embargo, no se pudo confirmar significancia estadística entre la presencia de esta bacteria y la presencia de displasia en LPO.

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

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.

Potential association between Fusobacterium nucleatum enrichment on oral mucosal surface and oral lichen planus.

OBJECTIVE: We determined the bacterial community structure of the buccal mucosa in patients with oral lichen planus (OLP) and evaluated the potential association of Fusobacterium nucleatum with OLP. SUBJECTS AND METHODS: We collected buccal mucosal swab samples of patients with OLP (n = 20) and healthy controls (n = 10) and performed 16S rRNA gene sequencing and real-time PCR to determine potentially different bacteria. Damaged and adjacent non-damaged mucosal swab samples of 25 OLP patients were used to detect the amount of F. nucleatum by real-time PCR. RESULTS: Compared with healthy controls, enrichment of Fusobacterium and Granulicatella was more abundant in patients with OLP (p = .0146 and 0.0034). The abundance of Fusobacterium and F. nucleatum was significantly enriched on buccal mucosa of patients with OLP compared with healthy controls (p = .0043 and 0.0235). Compared with adjacent non-damaged buccal mucosa of OLP patients, the amount of F. nucleatum in the damaged mucosa was significantly increased (p = .001). We examined third-level KEGG pathways for bacteria on mucosal surface and found that genes controlling sporulation and ether lipid metabolism were enriched in patients with OLP. CONCLUSIONS: A high amount of F. nucleatum may be associated with OLP. Further studies are required to investigate the precise association of F. nucleatum with OLP.

Cytokines Levels and Salivary Microbiome Play A Potential Role in Oral Lichen Planus Diagnosis.

Oral lichen planus (OLP) is a chronic Th1-mediated inflammatory mucocutaneous disease of the skin and oral mucosa that can have various clinical presentations. Lesions are usually bilateral and often painful. While cutaneous Lichen Planus (LP) lesions are self-limiting, the oral lesions are chronic and rarely remissive. The diagnosis of oral lichen planus (OLP) is often challenging, and confirmation by histopathological criterion is generally advised. The aim of our study was to identify the cytokines present in OLP-suggestive lesions and in non-specific inflammatory lesions (NSIL) used as controls. Moreover, assess cytokines protein levels and oral microbiota composition in whole saliva samples. Histopathological analysis, immunohistochemistry and gene expression were used as techniques to analyze the oral mucosal tissue samples. ELISA was conducted to analyze salivary cytokine levels and 16S rRNA sequencing was used to determine the salivary microbiome. As a result we observed larger number of infiltrated lymphocytes (p = 0.025), as well, more T CD4 lymphocytes in the epithelial tissue (p = 0.006) in OLP samples compared to NSIL. In addition, the OLP samples displayed more apoptotic cells compared to NSIL (p = 0.047). Regarding the cytokine analysis, IFN-γ and IL-33 were more expressed in OLP lesions than in NSIL samples (p < 0.001; p = 0.026). Furthermore, our results demonstrated higher levels of IFN-γ protein expression in the saliva of OLP group compared to controls (p = 0.0156). We also observed noted differences in the oral microbiota composition between OLP and NSIL saliva samples. In conclusion, OLP lesions presented larger numbers of apoptotic and inflammatory cells, higher levels of IFN-γ and IL-33 compared to NSIL, and these lesions also differ regarding oral microbiota composition. These results are consistent with the Th-1-mediated chronic inflammation nature of oral lichen planus investigated lesions and displayed unique features that could be used as a diagnostic tool.

Salivary mycobiome dysbiosis and its potential impact on bacteriome shifts and host immunity in oral lichen planus.

The biodiversity of the mycobiome, an important component of the oral microbial community, and the roles of fungal-bacterial and fungal-immune system interactions in the pathogenesis of oral lichen planus (OLP) remain largely uncharacterized. In this study, we sequenced the salivary mycobiome and bacteriome associated with OLP. First, we described the dysbiosis of the microbiome in OLP patients, which exhibits lower levels of fungi and higher levels of bacteria. Significantly higher abundances of the fungi Candida and Aspergillus in patients with reticular OLP and of Alternaria and Sclerotiniaceae_unidentified in patients with erosive OLP were observed compared to the healthy controls. Aspergillus was identified as an "OLP-associated" fungus because of its detection at a higher frequency than in the healthy controls. Second, the co-occurrence patterns of the salivary mycobiome-bacteriome demonstrated negative associations between specific fungal and bacterial taxa identified in the healthy controls, which diminished in the reticular OLP group and even became positive in the erosive OLP group. Moreover, the oral cavities of OLP patients were colonized by dysbiotic oral flora with lower ecological network complexity and decreased fungal-Firmicutes and increased fungal-Bacteroidetes sub-networks. Third, several keystone fungal genera (Bovista, Erysiphe, Psathyrella, etc.) demonstrated significant correlations with clinical scores and IL-17 levels. Thus, we established that fungal dysbiosis is associated with the aggravation of OLP. Fungal dysbiosis could alter the salivary bacteriome or may reflect a direct effect of host immunity, which participates in OLP pathogenesis.

The oral microbiome in oral lichen planus during a 1-year randomized clinical trial.

BACKGROUND: Several recent studies have investigated the oral bacteriome in oral lichen planus (OLP), but longitudinal changes in microbiome have not been investigated. OBJECTIVE: To study the bacteriome and mycobiome in OLP over a 1-year period and the impact of topical treatment. MATERIAL AND METHODS: Samples from 22 symptomatic OLP patients from a double-blinded, randomized intervention study were collected over a 1-year course at five visits. Bacterial and fungal abundances were investigated through lesional cytobrush (CB) and full mouthwash (MW). Initially, all patients received conventional (antimycotic or steroid) and probiotic or placebo treatment. RESULTS: The microbial composition differed between the MW and CB samples. During the study period, the microbial composition was individual, with pronounced variability between visits. Patients grouped according to initial conventional treatment. During the study period, unidirectional change in the bacteriome was seen in the antimycotic group, whereas the mycobiome was stable. Malassezia restricta was the most abundant fungus. CONCLUSIONS: The microbial composition of MW and CB differs in OLP. CB composition is less influenced by conventional and probiotic intervention. Initial antimycotic treatment influenced the bacteriome during the 1-year period. How the oral microbiome in health and disease is influenced by individual variability of fungi and bacteria, and Malassezia needs further investigation.

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

BACKGROUND: Oral 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. METHODS: Primary 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. RESULTS: OLP 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). CONCLUSION: OLP AFs demonstrated α-SMA expression and secreted pro-inflammatory cytokines in response to pg. LPS stimulation.

Candida species in patients with oral dysesthesia: A comparison of carriage among oral disease states.

OBJECTIVES: Oral dysesthesia (burning mouth syndrome) is characterized by a burning-like sensation of the oral mucosa. The etiology of this disorder is still unknown, however, associations with oral fungal carriage have been proposed and applied clinically. The aim of the this study was to compare oral Candida carriage in patients with oral dysesthesia with Candida carriage in patients with other commonly diagnosed oral diseases to clarify the relationship between Candida and oral dysesthesia. SUBJECTS AND METHODS: In total, 441 patients in total including 79 patients diagnosed with oral dysesthesia were included in this study. A retrospective analysis of mycological investigations undertaken in patients with clinically diagnosed oral dysesthesia compared with other oral conditions was undertaken. RESULTS: Oral carriage of Candida was found in 63.3% (50 of 79) of patients with oral dysesthesia. The frequency of carriage and oral load of Candida were not significantly increased in patients with oral dysesthesia relative to the other conditions assessed. Patients with clinical signs of fungal infection or xerostomia presented with increased carriage of Candida. CONCLUSION: There is no association between oral dysesthesia and the presence or load of oral Candida.

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

Oral 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.

Immunohistochemical detection of Mycoplasma salivarium in oral lichen planus tissue.

BACKGROUND: Oral lichen planus (OLP) is a T-cell-mediated inflammatory disease; however, its exact etiology is unknown. Hyperkeratosis is often observed in OLP lesions. Previous studies have revealed the localization of Mycoplasma salivarium in the epithelial cells of oral leukoplakia with hyperkeratosis. Herein, we investigated the presence of M. salivarium in OLP tissue by immunohistochemistry to determine the causative factor of OLP. METHODS: Forty-one formalin-fixed, paraffin-embedded samples obtained from 31 patients with OLP were examined. Ten samples of normal-appearing oral mucosa were used as controls. Immunohistochemistry (IHC) was performed using anti-M. salivarium monoclonal antibodies. RESULTS AND CONCLUSIONS: Mycoplasma salivarium was detected in the epithelium and lymphocyte infiltrate area in 24 of 41 OLP samples (58.5%). The bacteria were intracellularly localized in epithelial cells, while it was unclear whether they were also localized in lymphocyte cells or in the extracellular spaces among the lymphocytes in the subepithelial lymphocyte infiltrate area. Little or no staining was observed in the epithelium in the normal-appearing mucosa samples. Sawtooth rete ridge formation was observed in 21 OLP samples (51.2%), and a significant positive correlation between sawtooth rete ridge formation and IHC positivity was demonstrated. However, the role of M. salivarium in the epithelium and lamina propria of OLP tissue remains unknown.

Dysbiosis of oral buccal mucosa microbiota in patients with oral lichen planus.

OBJECTIVE: The bacterial community structure of buccal mucosa in patients with oral lichen planus was evaluated and compared with healthy control. SUBJECTS AND METHODS: Buccal scraping samples have been taken on 43 oral lichen planus patients (21 erosive and 22 non-erosive) and 21 mucosal healthy volunteers. The V3 hypervariable 16S rDNA region was amplified and sequenced by high-throughput 454 pyrosequencing. RESULTS: 94.26% of the total buccal bacteria were classified into 15 abundant genera. Eight of these abundant genera could be detected in all cases, namely Streptococcus, Prevotella, Haemophilu, Neisseria, Fusobacterium, Leptotrichia, Veillonella and Actinomyces. Four abundant bacteria showed significantly different prevalence at the genus level: Streptococcus was more abundant (P < 0.01) in healthy control group, while Fusobacterium (P < 0.01), Leptotrichia (P < 0.001) and Lautropia (P < 0.001) showed higher abundance in OLP group. Few differences can be found between erosive and non-erosive OLP. In general, 19 'core' OTUs at three levels were defined to be OLP specific, comparing with healthy control group. CONCLUSIONS: These results suggest that OLP is associated with dysbiosis of the oral microbiome. Further studies should be taken to elucidate the inner relationship between these observed changes and OLP development.

The presence of bacteria within tissue provides insights into the pathogenesis of oral lichen planus.

Oral lichen planus (OLP) is a chronic T cell-mediated mucocutaneous disease of unknown etiopathogenesis. Although various antigens have been considered, what actually triggers the inflammatory response of T cells is unknown. In the present study, we propose that intracellular bacteria present within tissues trigger T cell infiltration and provide target antigens. Sections of OLP (n = 36) and normal (n = 10) oral mucosal tissues were subjected to in situ hybridization using a universal probe targeting the bacterial 16S rRNA gene and immunohistochemistry with anti-CD3, anti-CD4, anti-CD8, and anti-macrophage-specific antibodies. Bacteria were abundant throughout the epithelium and the lamina propria of OLP tissues, which exhibited positive correlations with the levels of infiltrated CD3(+), CD4(+), and CD8(+) cells. Furthermore, bacteria were detected within the infiltrated T cells. Pyrosequencing analysis of the mucosal microbiota from OLP patients (n = 13) and control subjects (n = 11) revealed a decrease in Streptococcus and increases in gingivitis/periodontitis-associated bacteria in OLP lesions. Using the selected bacterial species, we demonstrated that certain oral bacteria damage the epithelial physical barrier, are internalized into epithelial cells or T cells, and induce production of T cell chemokines CXCL10 and CCL5. Our findings provide insights into the pathogenesis of OLP.

Preliminary analysis of salivary microbiome and their potential roles in oral lichen planus.

Several studies have explored the origin and development mechanism of oral lichen planus (OLP) with limited attention to the role of bacteria in the progression of this common oral disease. Here we utilized MiSeq sequencing of 16S rRNA gene amplicons to identify complex oral microbiota associated with OLP from saliva samples of two subtypes (reticular and erosive) of OLP patients and healthy controls. Our analyses indicated that the overall structure of the salivary microbiome was not significantly affected by disease status. However, we did observe evident variations in abundance for several taxonomic groups in OLP. Porphyromonas and Solobacterium showed significantly higher relative abundances, whereas Haemophilus, Corynebacterium, Cellulosimicrobium and Campylobacter showed lower abundances in OLP patients, as compared with healthy controls. In addition, we explored specific microbial co-occurrence patterns in OLP, and revealed significantly fewer linkers of Streptococcus comprising species in erosive OLP. Furthermore, the disease severity and immune dysregulation were also genus-associated, including with Porphyromonas that correlated to disease scores and salivary levels of interleukin (IL)-17 and IL-23. Overall, this study provides a general description of oral microbiome in OLP, and it will be useful for further investigation of their potential roles in the initiation and immune modulation of OLP.