Emerging evidence indicates that CCN1 is a novel inflammation-regulated mediator involved in the pathogenesis of some immune-mediated inflammatory diseases. The objective of this study was to investigate the preliminary roles of CCN1 and its related cytokines IL-1β, CCL5, and ICAM1 in oral lichen planus (OLP).CCN1 expression levels in biopsies from OLP patients against normal oral mucosa (NOM) using immunohistochemistry (42 OLP vs 9 NOM) and RT-qPCR (20 OLP vs 20 NOM) were compared, respectively. The correlation of CCN1 and IL-1β, CCL5, and ICAM1 expression was examined by RT-qPCR in tissue samples and an in vitro cell culture system using keratinocyte HaCaT cells incubated with lipopolysaccharides.Immunohistochemistry showed that CCN1 protein mainly expressed in the cytoplasm of epithelial keratinocytes of OLP. Consistently, RT-qPCR revealed that mRNA expression of CCN1 was increased in OLP compared with NOM (P < .05) and positively correlated with the high expression of IL-1β, ICAM1, and CCL5 (P < .001), respectively. Importantly, an in vitro study showed that keratinocyte proliferation significantly (P < .05) increased by CCN1 stimulation. Moreover, IL-1β, ICAM1, and CCL5 expression in keratinocytes stimulated by CCN1 was increased (P < .05), respectively.This preliminary study for the first time reported that altered expression of CCN1 was associated with high expression of IL-1β, ICAM1, and CCL5 in OLP. And we demonstrated CCN1 promoted keratinocyte activation, as well as IL-1β, ICAM1, and CCL5 production in keratinocytes. Our data indicated that the potential role of CCN1 and its related cytokines was involved in the pathogenesis of OLP.
Staphylococcus aureus, or methicillin-resistant Staphylococcus aureus (MRSA), is the predominant pathogen in skin and soft tissue infections (SSTIs), and MRSA membrane vesicles (MVs) play a pivotal role in bacterial pathogenesis and the modulation of the host immune response. We aimed to investigate the interaction between MRSA MVs and epithelial cells. In this study, MVs were isolated from an MRSA culture supernatant using the ELD method, comprising an electrophoretic technique used in combination with a 300 kDa cut-off dialysis bag. The proteomic analysis of the MRSA MVs via mass spectrometry showed that shared and distinct proteins exist in the MVs from clinical MRSA isolates with different genetic backgrounds, such as health-care-associated MRSA (HA-MRSA) and community-associated MRSA (CA-MRSA). These MRSA MVs were found to suppress the proliferation and increase the apoptosis of HaCaT cells. We conducted qPCR array, quantitative real-time PCR (qRT-PCR), and Western blotting (WB) analyses, and the results indicated that BCL2 antagonist/killer 1 (Bak1) may be involved in the apoptosis of HaCaT epithelial cells. Our findings suggest that MRSA MVs inhibit the proliferation and induce the apoptosis of epithelial cells.
Abstract Background Burning mouth syndrome (BMS) is a complex chronic pain disorder that significantly impairs patients' quality of life. Low-level laser therapy (LLLT) uses infrared or near-infrared light to produce analgesic, anti-inflammatory, and biological stimulation effects. The aim of this systematic review is to evaluate the effect of LLLT on burning pain, quality of life, and negative emotions in patients with BMS. Methods The PubMed, Embase, Cumulative Index of Nursing and Allied Health Literature (CINAHL), Cochrane Library, Web of Science, and Scopus databases were searched up January 2023 to identify relevant articles. All randomized controlled trials that were published in English and examined the use of LLLT treatment for BMS were included. The methodological quality of the included trials was assessed using the Cochrane risk of bias tool for randomized controlled trials (RCTs). A meta-analysis was performed to evaluate burning pain, quality of life, and negative emotions. Sensitivity, subgroup, and funnel plot analyses were also carried out. Results Fourteen RCTs involving a total of 550 patients with BMS met the inclusion criteria. The results showed that LLLT (measured by the Visual Analog Scale; SMD: -0.87, 95% CI: -1.29 to -0.45, P < 0.001) was more effective for reducing burning pain than placebo LLLT or clonazepam. LLLT improved quality of life (evaluated by the Oral Health Impact Profile-14; SMD: 0.01, 95% CI: -0.58 to 0.60, P = 0.97) and negative emotions (evaluated by the Hospital Anxiety and Depression Scale; SMD: -0.12, 95% CI: -0.54 to 0.30, P = 0.59), but these effects were not statistically significant. Conclusions The meta-analysis revealed that LLLT may be an effective therapy for improving burning pain in patients with BMS, and producing a positive influence on quality of life and negative emotions. A long-term course of intervention, a larger sample size, and a multidisciplinary intervention design are urgently needed in future research. Trial registration PROSPERO registration number: CRD42022308770.
MicroRNA-27b (miR-27b) was recently found to be significantly downregulated in oral lichen planus (OLP). However, evidence of the function of miR-27b in OLP remains limited.Initially, miR-27b expression in OLP was verified using the quantitative real-time polymerase chain reaction (qRT-PCR). Functionally, gain-/loss-of-function studies were then conducted using miR-27b mimics/inhibitor to investigate cell growth in human oral keratinocytes (HOKs). Mechanistically, subsequent miRNA target analyses including a starBase database analysis and a luciferase reporter assay were performed to predict and validate the direct target, respectively. In addition, overexpression/knockdown assays of target(s) of miR-27b were performed to investigate its functional significance and qRT-PCR and western blotting were used to evaluate the target(s) of miR-27b mRNA and protein levels, respectively.MicroRNA-27b was significantly downregulated in OLP tissues when compared with healthy control tissues. Bioinformatics predicted that Polo Like Kinase 2 (PLK2) might be a potential target of miR-27b, while the luciferase reporter assay results showed the direct inhibition of the plk2-3'untranslated region by miR-27b. Moreover, functional analysis indicated that downregulated miR-27b caused an increase in cell growth in HOKs, and correspondingly, overexpression of PLK2 promoted HOK proliferation.There were aberrant expressions of miR-27b and PLK2 in OLP tissues. Decreased miR-27b may have induced cell proliferation by increasing the levels of PLK2 in HOKs, which provides a new perspective into the potential mechanisms underlying OLP development.
Abstract 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.
Abstract Oral lichen planus (OLP) is considered a precancerous lesion with no known cure. Recent studies reported that abnormal regulation of apoptosis was involved in the pathogenesis of OLP. Next generation sequencing was used to screen the candidate microRNAs and genes in biopsies from patients with OLP and healthy mucosa. Human oral keratinocytes were transfected into the related oligonucleotides of miR‐27b‐3p/cyclophilin D and their control groups. Apoptosis was detected by TdT‐mediated dUTP nick end labelling and flow cytometry. The levels of mRNA and protein were detected by quantitative PCR, Western blots, and enzyme‐linked immunosorbent assays, respectively. Luciferase assays were performed to detect the luciferase activities of miR‐27b‐3p and cyclophilin D. Here, we showed that basal epithelium apoptosis was reduced and the miR‐27b‐3p levels were decreased in clinical OLP samples. We also found that down‐regulation of miR‐27b‐3p inhibited epithelial keratinocyte apoptosis by up‐regulating cyclophilin D expression. Moreover, cyclophilin D increased the protein stability of Bcl2 through direct binding, and Bcl2 suppressed caspase9/3 activation and cytochrome C release. Taken together, these data showed that miR‐27b‐3p regulated keratinocyte apoptosis through cyclophilin D/Bcl2 signalling, suggesting the miR‐27b‐3p regulated the pathogenesis of OLP.
To assess potential association between oral nevi (ON) and nevus-associated melanoma (NAM), in which melanoma cells coexist with nevus cells.A total of 74 ON patients and 7 NAM patients were retrospectively reviewed. Comparative and regression analyses of clinical and histological data were performed between two groups.The mean age of the patients with ON was 36.5 years compared with that of 54.7 years of the patients with NAM (p = .008). Gender ratio was female predominance for ON (1.64:1 ratio) and male predominance for NAM (6:1 ratio). The most common location of ON and NAM was the palate (31.1%) and gingiva (71.4%), respectively. Univariate regression analysis revealed that elderly male patients (≥60 years) with junctional ON located on the gingiva correlate with higher risk of melanoma. Multivariate analysis revealed that junctional type of ON was an independent factor (adjusted OR, 38.32; 95% CI, 3.20-458.64; p = .004) associated significantly with increased risk for melanoma.The preliminary study for the first time elucidated the clinicopathologic features of a Chinese series of ON and evaluated the potential association between ON and NAM with a limited sample size. Further large multicenter studies are needed to confirm the findings.
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