Laugier–Hunziker syndrome (LHS) is an acquired pigmentary condition affecting lips, oral mucosa and acral area, frequently associated with longitudinal melanonychia. There is neither malignant predisposition nor underlying systemic abnormality associated with LHS. Herein, we present three uncommon cases of LHS with possibly new feature of nail pigmentation, which were diagnosed during the past 2 years. We also review the clinical and histological findings, differential diagnosis, and treatment of the syndrome in published literature.

Recent studies show that NK cells play important roles in murine biliary atresia (BA), and a temporary immunological gap exists in this disease. In this study, we found high-mobility group box-1 (HMGB1) and TLRs were overexpressed in human and rotavirus-induced murine BA. The overexpressed HMGB1 released from the nuclei of rotavirus-infected cholangiocytes, as well as macrophages, activated hepatic NK cells via HMGB1-TLRs-MAPK signaling pathways. Immature NK cells had low cytotoxicity on rotavirus-injured cholangiocytes due to low expression of TLRs, which caused persistent rotavirus infection in bile ducts. HMGB1 up-regulated the levels of TLRs of NK cells and promoted NK cell activation in an age-dependent fashion. As NK cells gained increasing activation as mice aged, they gained increasing cytotoxicity on rotavirus-infected cholangiocytes, which finally caused BA. Adult NK cells eliminated rotavirus-infected cholangiocytes shortly after infection, which prevented persistent rotavirus infection in bile ducts. Moreover, adoptive transfer of mature NK cells prior to rotavirus infection decreased the incidence of BA in newborn mice. Thus, the dysfunction of newborn NK cells may, in part, participate in the immunological gap in the development of rotavirus induced murine BA.

Labial and oral melanotic macules are commonly encountered in a broad range of conditions ranging from physiologic pigmentation to a sign of an underlying life-threatening disease. Although Laugier-Hunziker syndrome (LHS) shares some features of labial and oral pigmentation with a variety of conditions, it is a benign and acquired condition, frequently associated with longitudinal melanonychia. Herein, the demographic, clinical, dermoscopic, and pathological aspects of LHS were reviewed comprehensively. The important differential diagnoses of mucocutaneous and nail pigmentation are provided. An accurate diagnosis is crucial to design a reasonable medical strategy, including management options, malignant transformation surveillance, and psychological support. It is important that clinicians conduct long-term follow-up and surveillance due to the potential risks of malignant transformation and local severe complications in some conditions.

Oral immunosuppression caused by smoking creates a microenvironment to promote the occurrence and development of oral mucosa precancerous lesions. This study aimed to investigate the role of metabolism and macrophage polarization in cigarette-promoting oral leukoplakia. The effects of cigarette smoke extract (CSE) on macrophage polarization and metabolism were studied in vivo and in vitro. The polarity of macrophages was detected by flow cytometric analysis and qPCR. Liquid chromatography-mass spectrometry (LC-MS) was used to perform a metabolomic analysis of Raw cells stimulated with CSE. Immunofluorescence and flow cytometry were used to detect the polarity of macrophages in the condition of glutamine abundance and deficiency. Cell Counting Kit-8 (CCK-8), wound-healing assay, and Annexin V-FITC (fluorescein isothiocyanate)/PI (propidium iodide) double-staining flow cytometry were applied to detect the growth and transferability and apoptosis of Leuk-1 cells in the supernatant of Raw cells which were stimulated with CSE, glutamine abundance and deficiency. Hyperkeratosis and dysplasia of the epithelium were evident in smoking mice. M2 macrophages increased under CSE stimulation in vivo and in vitro. In total, 162 types of metabolites were detected in the CSE group. The metabolites of nicotine, glutamate, arachidic acid, and arginine changed significantly. The significant enrichment pathways were also selected, including nicotine addiction, glutamine and glutamate metabolism, and arginine biosynthesis. The results also showed that the supernatant of Raw cells stimulated by CSE could induce excessive proliferation of Leuk-1 and inhibit apoptosis. Glutamine abundance can facilitate this process. Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and macrophage M2 polarization.

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In many caries-promoting Streptococcus species, glucosyltransferases (Gtfs) are recognized as key enzymes contributing to the modification of biofilm structures, disruption of homeostasis of healthy microbiota community and induction of caries development. It is therefore of great interest to investigate how Gtf genes have evolved in Streptococcus. In this study, we conducted a comprehensive survey of Gtf genes among 872 streptococci genomes of 37 species and identified Gtf genes from 364 genomes of 18 species. To clarify the relationships of these Gtf genes, 45 representative sequences were used for phylogenic analysis, which revealed two clear clades. Clade I included 12 Gtf genes from nine caries-promoting species of the Mutans and Downei groups, which produce enzymes known to synthesize sticky, water-insoluble glucans (WIG) that are critical for modifying biofilm structures. Clade II primarily contained Gtf genes responsible for synthesizing water-soluble glucans (WSG) from all 18 species, and this clade further diverged into three subclades (IIA, IIB, and IIC). An analysis of 16 pairs of duplicated Gtf genes revealed high divergence levels at the C-terminal repeat regions, with ratios of the non-synonymous substitution rate (dN) to synonymous substitution rate (dS) ranging from 0.60 to 1.03, indicating an overall relaxed constraint in this region. However, among the clade I Gtf genes, some individual repeat units possessed strong functional constraints by the same criterion. Structural variations in the repeat regions were also observed, with detection of deletions or recent duplications of individual repeat units. Overall, by establishing an updated phylogeny and further elucidating their evolutionary patterns, this work enabled us to gain a greater understanding of the origination and divergence of Gtf genes in Streptococcus.

The aim of this study is to investigate protective effects of sesaminol on the human bronchial epithelial (BEAS-2B) cell line against oxidative damage of cigarette smoke extract (CSE). BEAS-2B cells were pre-incubated with sesaminol for 12 h and then treated with various concentrations of CSE for 24 h. After that proliferation ability, levels of reactive oxygen species (ROS) and lactate dehydrogenase (LDH), cell apoptosis, activities of catalase (CAT) and superoxide dismutase (SOD), and mRNA levels of IL-8 and IL-6 were measured. The results showed that sesaminol significantly improved BEAS-2B cell viability, reduced the production of ROS and LDH of cells, inhibited cell apoptosis and increased CAT and SOD activities in CSE-treated cells. Sesaminol also inhibited the expression of IL-8 and IL-6 mRNA following CSE exposure. In conclusion, sesaminol may protect BEAS-2B cells against CSE-induced oxidative damage.

BackgroundCigarette smoke a recognized risk factor for many systemic diseases and also oral diseases. Human beta defensins (HBDs), a group of important antimicrobial peptides expressed by the epithelium, are crucial for local defense and tissue homeostasis of oral cavity. The aim of this study was to evaluate potential effects of whole cigarette smoke (WCS) exposure on the expression and secretion of HBDs by oral mucosal epithelial cells.MethodsImmortalized human oral mucosal epithelial (Leuk-1) cells were exposed to WCS for various time periods. HBD-1, -2 and -3 expression and subcellular localization were detected by real time qPCR, immunofluorescence assay and confocal microscopy. According to the relative fluorescent intensity, the expression levels of HBD-1, -2 and -3 were evaluated by digital image analysis system. The alteration of HBD-1, -2 and -3 secretion levels was measured by the Enzyme-Linked Immunosorbent Assay.ResultsWCS exposure remarkably attenuated HBD-1 expression and secretion while clearly enhanced HBD-2, -3 expression levels and HBD-2 secretion by Leuk-l cells. It appeared that there was no significant effect of WCS exposure on HBD-3 secretion.ConclusionsWCS exposure could modulate expression and secretion of HBDs by oral mucosal epithelial cells, establishing a link between cigarette smoke and abnormal levels of antimicrobial peptides. The present results may give a new perspective to investigate smoking-related local defense suppression and oral disease occurrence.