Emerging Role of the Mast Cell-Microbiota Crosstalk in Cutaneous Homeostasis and Immunity.

The skin presents a multifaceted microbiome, a balanced coexistence of bacteria, fungi, and viruses. These resident microorganisms are fundamental in upholding skin health by both countering detrimental pathogens and working in tandem with the skin's immunity. Disruptions in this balance, known as dysbiosis, can lead to disorders like psoriasis and atopic dermatitis. Central to the skin's defense system are mast cells. These are strategically positioned within the skin layers, primed for rapid response to any potential foreign threats. Recent investigations have started to unravel the complex interplay between these mast cells and the diverse entities within the skin's microbiome. This relationship, especially during times of both balance and imbalance, is proving to be more integral to skin health than previously recognized. In this review, we illuminate the latest findings on the ties between mast cells and commensal skin microorganisms, shedding light on their combined effects on skin health and maladies.

Impact of Gut Bacterial Metabolites on Psoriasis and Psoriatic Arthritis: Current Status and Future Perspectives.

There is growing evidence that supports a role of gut dysbiosis in the pathogenesis of psoriasis (Pso). Thus, probiotic supplementation and fecal microbiota transplantation may serve as promising preventive and therapeutic strategies for patients with Pso. One of the basic mechanisms through which the gut microbiota interacts with the host is through bacteria-derived metabolites, usually intermediate or end products produced by microbial metabolism. In this study, we provide an up-to-date review of the most recent literature on microbial-derived metabolites and highlight their roles in the immune system, with a special focus on Pso and one of its most common comorbidities, psoriatic arthritis.

Evaluation of the effects of Lake Hévíz sulfur thermal water on skin microbiome in plaque psoriasis: An open label, pilot study.

Psoriasis is a chronic inflammatory skin disease. It is associated with changes in skin microbiome. The aim of this study was to evaluate how Lake Hévíz sulfur thermal water influences the composition of microbial communities that colonizes skin in patients with psoriasis. Our secondary objective was to investigate the effects of balneotherapy on disease activity. In this open label study, participants with plaque psoriasis underwent 30-min therapy sessions in Lake Hévíz, at a temperature of 36 °C, five times a week for 3 weeks. The skin microbiome samples were collected by swabbing method from two different areas (lesional skin-psoriatic plaque and non-lesional skin). From 16 patients, 64 samples were processed for a 16S rRNA sequence-based microbiome analysis. Outcome measures were alpha-diversity (Shannon, Simpson, and Chao1 indexes), beta-diversity (Bray-Curtis metric), differences in genus level abundances, and Psoriasis Area and Severity Index (PASI). Skin microbiome samples were collected at baseline, and immediately after treatment. Based on the visual examination of the employed alpha- and beta-diversity measures, no systematic difference based on sampling timepoint or sample location could be revealed in these regards. Balneotherapy in the unaffected area significantly increased the level of Leptolyngbya genus, and significantly decreased the level of Flavobacterium genus. A similar trend was revealed by the results of the psoriasis samples, but the differences were not statistically significant. In patients with mild psoriasis, a significant improvement was observed in PASI scores.

The effects of Malassezia in the activation of Interleukin (IL)-23/IL-17 axis in Psoriasis.

We explore the association of Malassezia and IL-23/IL-17 axis in the skin lesions of patients with Psoriasis. From October 2018 to October 2020, 202 psoriasis patients were hospitalized in the dermatology department of Yantaishan hospital. The patients' skin lesions were collected, and Malassezia-specific mRNA in the skin lesions was determined. The patients were subdivided into Malassezia high and low distribution groups as per the Malassezia-specific mRNA results. Psoriasis Area and Severity Index (PASI) scores between the two groups were performed. LL-37, IL-23, IL-17A, and tumor necrosis factor α (TNF-α) expression in the skin lesions of the two groups were determined. Malassezia mRNA and the correlation of LL-37 with inflammatory factors TNF-α, IL-23, and IL-17A were determined. The relevance of inflammatory factors, Malassezia infection, and LL-37 content with PASI score were studied. The Malassezia high distribution group was treated with etoconazole, and the effects of treatment on the PASI score, IL-23, TNF-α, and IL-17A were determined. The PASI score, neutrophil, eosinophil, and peripheral blood white blood cell counts, and lgG in the Malassezia high distribution group were significantly higher than in the low distribution group (P<0.05). IL-23, LL-37, TNF-α, and IL-17A levels in the Malassezia high distribution group were significantly higher than in the low distribution group (P<0.05). Malassezia and LL-37 levels had a moderate positive correlation (R=0.5009, P<0.0001). Malassezia and LL-37, IL-17A, TNF-a, and IL- 23 correlated positively. Malassezia, IL-17A, LL37, TNF-a, and IL-23 correlated positively with the PASI score of Psoriasis. Ketoconazole therapy inhibited the PASI score, IL-23, TNF-a, and IL-17A expressions in patients. Malassezia enhances the progression of Psoriasis through the aberrant activation of the IL-23/IL-17 axis.

Group IIA secreted phospholipase A2 controls skin carcinogenesis and psoriasis by shaping the gut microbiota.

Besides promoting inflammation by mobilizing lipid mediators, group IIA secreted phospholipase A2 (sPLA2-IIA) prevents bacterial infection by degrading bacterial membranes. Here, we show that, despite the restricted intestinal expression of sPLA2-IIA in BALB/c mice, its genetic deletion leads to amelioration of cancer and exacerbation of psoriasis in distal skin. Intestinal expression of sPLA2-IIA is reduced after treatment with antibiotics or under germ-free conditions, suggesting its upregulation by gut microbiota. Metagenome, transcriptome, and metabolome analyses have revealed that sPLA2-IIA deficiency alters the gut microbiota, accompanied by notable changes in the intestinal expression of genes related to immunity and metabolism, as well as in the levels of various blood metabolites and fecal bacterial lipids, suggesting that sPLA2-IIA contributes to shaping of the gut microbiota. The skin phenotypes in Pla2g2a-/- mice are lost (a) when they are cohoused with littermate WT mice, resulting in the mixing of the microbiota between the genotypes, or (b) when they are housed in a more stringent pathogen-free facility, where Pla2g2a expression in WT mice is low and the gut microbial compositions in both genotypes are nearly identical. Thus, our results highlight a potentially new aspect of sPLA2-IIA as a modulator of gut microbiota, perturbation of which affects distal skin responses.

Prevalence of Candida species in Psoriasis.

BACKGROUND: Psoriasis patients are more frequently colonised with Candida species. The correlation between fungal colonisation and clinical severity is unclear, but may exacerbate psoriasis and the impact of antipsoriatic therapies on the prevalence of Candida is unknown. OBJECTIVES: To examine the prevalence of C species in psoriasis patients compared to an age- and sex-matched control population, we investigated the influence of Candida colonisation on disease severity, immune cell activation and the interplay on psoriatic treatments. METHODS: The prevalence of C species was examined in 265 psoriasis patients and 200 control subjects by swabs and stool samples for fungal cultures. Peripheral mononuclear blood cells (PBMCs) were collected from 20 fungal colonised and 24 uncolonised patients and stimulated. The expression of interferon (IFN)-γ, IL-17A, IL-22 and tumour necrosis factor (TNF)-α from stimulated PBMCs was measured by quantitative real-time polymerase chain reaction (qPCR). RESULTS: A significantly higher prevalence for Candida was detected in psoriatic patients (p ≤ .001) compared to the control subjects; most abundant in stool samples, showing Candida albicans. Older participants (≥51 years) were more frequent colonised, and no correlation with gender, disease severity or systemic treatments like IL-17 inhibitors was found. CONCLUSIONS: Although Candida colonisation is significantly more common in patients with psoriasis, it does not influence the psoriatic disease or cytokine response. Our study showed that Candida colonisation is particularly more frequent in patients with psoriasis ≥51 years of age. Therefore, especially this group should be screened for symptoms of candidiasis during treatment with IL-17 inhibitors.

Overall Prevalence and Prevalence Compared among Psoriasis Treatments of Onychomycosis in Patients with Nail Psoriasis and Fungal Involvement.

BACKGROUND: Whether nail psoriasis can increase the risk of onychomycosis is still being debated, and data relating to the prevalence of onychomycosis among psoriasis patients receiving different treatments is limited. OBJECTIVES: To investigate the overall prevalence and prevalence compared among psoriasis treatments of onychomycosis in patients with nail psoriasis and fungal involvement. METHODS: A prospective study of three groups of nail psoriasis being treated with only topical medication, methotrexate, or biologics (25 patients per group, 150 nails) was conducted at Siriraj Hospital (Bangkok, Thailand) during November 2018 to September 2020. Demographic data, psoriasis severity, and nail psoriasis severity were recorded. The nail most severely affected with psoriasis on each hand was selected for mycological testing. Potassium hydroxide, periodic acid-Schiff stain, and fungal culture were performed. RESULTS: The prevalence of onychomycosis in nail psoriasis was 35.3%. Among the treatment groups, the prevalence of onychomycosis was significantly higher in the methotrexate group than in the topical treatment and biologic treatment groups (p = 0.014). Candida spp. was the main causative organism, followed by Trichophyton rubrum. Thumb was most commonly affected (59.3%). The most common abnormality of the nail matrix and the nail bed was pitted nail (71.3%) and onycholysis (91.3%), respectively. Multivariate analysis revealed diabetes, wet-work exposure, and methotrexate treatment to be predictors of onychomycosis. CONCLUSIONS: Several factors, including psoriasis treatment, were shown to increase the risk of onychomycosis in nail psoriasis. Further research is needed to determine whether biologic agents, especially interleukin-17 inhibitors, can increase risk of onychomycosis and Candida infection/colonization of the nails.

Compositional Features of Distinct Microbiota Base on Serum Extracellular Vesicle Metagenomics Analysis in Moderate to Severe Psoriasis Patients.

The bacterial microbiota in the skin and intestine of patients with psoriasis were different compared with that of healthy individuals. However, the presence of a distinct blood microbiome in patients with psoriasis is yet to be investigated. In this study, we investigated the differences in bacterial communities in plasma-derived extracellular vesicles (EVs) between patients with moderate to severe psoriasis (PSOs) and healthy controls (HCs). The plasma EVs from the PSO (PASI > 10) (n = 20) and HC (n = 8) groups were obtained via a series of centrifugations, and patterns were examined and confirmed using transmission electron microscopy (TEM) and EV-specific markers. The taxonomic composition of the microbiota was determined by using full-length 16S ribosomal RNA gene sequencing. The PSO group had lower bacterial diversity and richness compared with HC group. Principal coordinate analysis (PCoA)-based clustering was used to assess diversity and validated dysbiosis for both groups. Differences at the level of amplicon sequence variant (ASV) were observed, suggesting alterations in specific ASVs according to health conditions. The HC group had higher levels of the phylum Firmicutes and Fusobacteria than in the PSO group. The order Lactobacillales, family Brucellaceae, genera Streptococcus, and species Kingella oralis and Aquabacterium parvum were highly abundant in the HC group compared with the PSO group. Conversely, the order Bacillales and the genera Staphylococcus and Sphihgomonas, as well as Ralstonia insidiosa, were more abundant in the PSO group. We further predicted the microbiota functional capacities, which revealed significant differences between the PSO and HC groups. In addition to previous studies on microbiome changes in the skin and gut, we demonstrated compositional differences in the microbe-derived EVs in the plasma of PSO patients. Plasma EVs could be an indicator for assessing the composition of the microbiome of PSO patients.

The power and potential of BIOMAP to elucidate host-microbiome interplay in skin inflammatory diseases.

The two most common chronic inflammatory skin diseases are atopic dermatitis (AD) and psoriasis. The underpinnings of the remarkable degree of clinical heterogeneity of AD and psoriasis are poorly understood and, as a consequence, disease onset and progression are unpredictable and the optimal type and time point for intervention are as yet unknown. The BIOMAP project is the first IMI (Innovative Medicines Initiative) project dedicated to investigating the causes and mechanisms of AD and psoriasis and to identify potential biomarkers responsible for the variation in disease outcome. The consortium includes 7 large pharmaceutical companies and 25 non-industry partners including academia. Since there is mounting evidence supporting an important role for microbial exposures and our microbiota as factors mediating immune polarization and AD and psoriasis pathogenesis, an entire work package is dedicated to the investigation of skin and gut microbiome linked to AD or psoriasis. The large collaborative BIOMAP project will enable the integration of patient cohorts, data and knowledge in unprecedented proportions. The project has a unique opportunity with a potential to bridge and fill the gaps between current problems and solutions. This review highlights the power and potential of the BIOMAP project in the investigation of microbe-host interplay in AD and psoriasis.

Potential Role of Probiotics in Ameliorating Psoriasis by Modulating Gut Microbiota in Imiquimod-Induced Psoriasis-Like Mice.

Psoriasis is an immune-mediated systemic disease that may be treated with probiotics. In this study, probiotic strains that could or could not decrease interleukin (IL)-17 levels were applied to imiquimod (IMQ)-induced psoriasis-like mice via oral administration. Bifidobacteriumadolescentis CCFM667, B. breve CCFM1078, Lacticaseibacillusparacasei CCFM1074, and Limosilactobacillus reuteri CCFM1132 ameliorated psoriasis-like pathological characteristics and suppressed the release of IL-23/T helper cell 17 (Th17) axis-related inflammatory cytokines, whereas B. animalis CCFM1148, L. paracasei CCFM1147, and L. reuteri CCFM1040 neither alleviated the pathological characteristics nor reduced the levels of inflammatory cytokines. All effective strains increased the contents of short-chain fatty acids, which were negatively correlated with the levels of inflammatory cytokines. By performing 16S rRNA gene sequencing, the diversity of gut microbiota in psoriasis-like mice was found to decrease, but all effective strains made some specific changes to the composition of gut microbiota compared to the ineffective strains. Furthermore, except for B. breve CCFM1078, all other effective strains decreased the abundance of the family Rikenellaceae, which was positively correlated with psoriasis-like pathological characteristics and was negatively correlated with propionate levels. These findings demonstrated effects of strain-specificity, and how probiotics ameliorated psoriasis and provide new possibilities for the treatment of psoriasis.

Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated.

Psoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated information on pathogenesis, comorbidities, and therapy of psoriasis. The pathogenesis of psoriasis may involve the dysfunction of indoleamine 2,3-dioxygenase 2 or of UBA domain containing 1-mediated regulation of CARD14/CARMA2sh. The blood cells of psoriasis patients showed the enhanced oxidative stress/autophagy flux and decreased 20S proteasome activity. Elafin, clusterin, or selenoprotein P may act as biomarkers for psoriasis and comorbid metabolic diseases. The proteomic profile of psoriasis lesions showed the dysfunction of dermal fibroblasts; up-regulation of proinflammatory factors and signal transduction or down-regulation of structural molecules. The skin inflammation in psoriasis may populate certain gut bacteria, such as Staphylococcus aureus and Streptococcus danieliae, which worsen the skin inflammation in turn. The psoriasis-associated pruritus may be caused by immune, nervous, or vascular mechanisms. In addition to current oral treatments and biologics, a new treatment option for psoriasis is now being developed, such as retinoic-acid-receptor-related orphan nuclear receptor γt inhibitors, IL-36 receptor antagonist, or aryl hydrocarbon receptor agonist. Antimicrobial peptides and innate immune cells, involved in the pathogenesis of psoriasis, may be novel therapeutic targets. The pathomechanisms and responses to drugs in collagen diseases are partially shared with and partially different from those in psoriasis. Certain nutrients can exacerbate or regulate the progress of psoriasis. The articles in this Special Issue will encourage attractive approaches to psoriasis by future researchers.

Alterations of the Skin and Gut Microbiome in Psoriasis and Psoriatic Arthritis.

Numerous scientific studies in recent years have shown significant skin and gut dysbiosis among patients with psoriasis. A significant decrease in microbiome alpha-diversity (abundance of different bacterial taxa measured in one sample) as well as beta-diversity (microbial diversity in different samples) was noted in psoriasis skin. It has been proven that the representation of Cutibacterium, Burkholderia spp., and Lactobacilli is decreased and Corynebacterium kroppenstedii, Corynebacterium simulans, Neisseria spp., and Finegoldia spp. increased in the psoriasis skin in comparison to healthy skin. Alterations in the gut microbiome in psoriasis are similar to those observed in patients with inflammatory bowel disease. In those two diseases, the F. prausnitzii, Bifidobacterium spp., Lactobacillus spp., Parabacteroides and Coprobacillus were underrepresented, while the abundance of Salmonella sp., Campylobacter sp., Helicobacter sp., Escherichia coli, Alcaligenes sp., and Mycobacterium sp. was increased. Several research studies provided evidence for the significant influence of psoriasis treatments on the skin and gut microbiome and a positive influence of orally administered probiotics on the course of this dermatosis. Further research is needed to determine the influence of the microbiome on the development of inflammatory skin diseases. The changes in microbiome under psoriasis treatment can serve as a potential biomarker of positive response to the administered therapy.

Psoriasis and Gut Microbiome-Current State of Art.

Psoriasis is a chronic, immune-mediated inflammatory disease that affects around 125 million people worldwide. Several studies concerning the gut microbiota composition and its role in disease pathogenesis recently demonstrated significant alterations among psoriatic patients. Certain parameters such as Firmicutes/Bacteroidetes ratio or Psoriasis Microbiome Index were developed in order to distinguish between psoriatic and healthy individuals. The "leaky gut syndrome" and bacterial translocation is considered by some authors as a triggering factor for the onset of the disease, as it promotes chronic systemic inflammation. The alterations were also found to resemble those in inflammatory bowel diseases, obesity and certain cardiovascular diseases. Microbiota dysbiosis, depletion in SCFAs production, increased amount of produced TMAO, dysregulation of the pathways affecting the balance between lymphocytes populations seem to be the most significant findings concerning gut physiology in psoriatic patients. The gut microbiota may serve as a potential response-to-treatment biomarker in certain cases of biological treatment. Oral probiotics administration as well as fecal microbial transplantation were most reported in bringing health benefits to psoriatic patients. However, the issue of psoriatic bacterial gut composition, its role and healing potential needs further investigation. Here we reviewed the literature on the current state of the relationship between psoriasis and gut microbiome.

Non-alcoholic fatty liver disease is associated with bacterial translocation and a higher inflammation response in psoriatic patients.

Psoriasis and non-alcoholic fatty liver disease (NAFLD) are both inflammatory diseases. The study objective was to estimate the risk of NAFLD, non-alcoholic steatohepatitis, and liver fibrosis (by liver stiffness and liver biopsy) in patients with psoriasis and to determine the epidemiological, clinical, immunological (TNF-α, IL-2, IL-6, IL-12, IL-17, IL-23, and TGF-ß) characteristics, and bacterial translocation. Of the 215 psoriatic patients included, 91 presented NAFLD (prevalence: 42.3%). Compared to patients with psoriasis alone, those with NAFLD were significantly more likely to have metabolic syndrome, diabetes, dyslipidemia, body mass index ≥ 30 kg/m2, homeostatic model assessment of insulin resistance ≥ 2.15, and greater psoriasis area severity index. NAFLD patients also had significantly higher levels of TNF-α (p = 0.002) and TGF-ß (p = 0.007) and a higher prevalence of bacterial translocation (29.7% vs. 13.7%; p = 0.004). Liver stiffness measurement was over 7.8 kPa in 17.2% (15/87) of NAFLD patients; 13 of these underwent liver biopsy, and 5.7% (5/87) had liver fibrosis, while 1.1% (1/87) had advanced fibrosis or non-alcoholic steatohepatitis. In conclusion the prevalence of NAFLD in patients with psoriasis is high and associated with a higher prevalence of metabolic syndrome features, bacterial translocation and a higher pro-inflammatory state. It is worth mentioning that liver fibrosis and non-alcoholic steatohepatitis are not frequent in this population of patients.

Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients.

BACKGROUND: Psoriasis is an inflammatory skin disease associated with multiple comorbidities and substantially diminishes patients' quality of life. The gut microbiome has become a hot topic in psoriasis as it has been shown to affect both allergy and autoimmunity diseases in recent studies. Our objective was to identify differences in the fecal microbial composition of patients with psoriasis compared with healthy individuals to unravel the microbiota profiling in this autoimmune disease. RESULTS: We collected fecal samples from 30 psoriasis patients and 30 healthy controls, sequenced them by 16S rRNA high-throughput sequencing, and identified the gut microbial composition using bioinformatic analyses including Quantitative Insights into Microbial Ecology (QIIME) and Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt). Our results showed that different relative abundance of certain bacterial taxa between psoriasis patients and healthy individuals, including Faecalibacterium and Megamonas, were increased in patients with psoriasis. It's also implicated that many cytokines act as main effect molecules in the pathology of psoriasis. We selected the inflammation-related indicators that were abnormal in psoriasis patients and found the microbiome variations were associated with the level of them, especially interleukin-2 receptor showed a positive relationship with Phascolarctobacterium and a negative relationship with the Dialister. The relative abundance of Phascolarctobacterium and Dialister can be regard as predictors of psoriasis activity. The correlation analysis based on microbiota and Inflammation-related indicators showed that microbiota dysbiosis might induce an abnormal immune response in psoriasis. CONCLUSIONS: We concluded that the gut microbiome composition in psoriasis patients has been altered markedly and provides evidence to understand the relationship between gut microbiota and psoriasis. More mechanistic experiments are needed to determine whether the differences observed in gut microbiota are the cause or consequences of psoriasis and whether the relationship between gut microbiota and cytokines was involved.

Dysregulation of the gut-brain-skin axis and key overlapping inflammatory and immune mechanisms of psoriasis and depression.

The occurrence, progression and recurrence of psoriasis are thought to be related to mood and psychological disorders such as depression. Psoriasis can lead to depression, and depression, in turn, exacerbates psoriasis. No specific mechanism can explain the association between psoriasis and depression. The gut-brain-skin axis has been used to explain correlations among the gut microbiota, emotional states and systemic and skin inflammation, and this axis may be associated with overlapping mechanisms between psoriasis and depression. Therefore, in the context of the gut-brain-skin axis, we systematically summarized and comparatively analysed the inflammatory and immune mechanisms of psoriasis and depression and illustrated the dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and the gut microbiota. This review provides a theoretical basis and new targets for the treatment of psoriasis and depression.

Distribution of Malassezia species on the skin of patients with psoriasis.

INTRODUCTION: Malassezia species can induce the expression of interleukin-17 (IL-17), which plays an important role in the inflammatory and immune response in psoriasis (PS). The purpose of this study was to investigate the Malassezia species composition in patients with PS and healthy individuals and explore the role of Malassezia species in the pathogenesis of PS. MATERIALS AND METHODS: A total of 28 patients with PS and 10 age- and sex-matched healthy individuals participated in this study. Specimens collected from the lesional and non-lesional skin of patients with PS and the skin of healthy individuals were analyzed by using nested PCR. RESULTS: The relative abundance of Malassezia species was 84.96% in healthy subjects, more than twice that in patients with PS (P<0.01). M. restricta (43.09%) and M. globosa (41.38%) were the main Malassezia species in patients with PS followed by M. furfur (4.84%) and M. sympodialis (2.49%). M. sympodialis accounted for 18. 81% of the Malassezia species in healthy subjects, which was nearly eight times higher than in patients with PS (P<0.01). Further, M. furfur was detected both on lesional and non-lesional psoriatic skin, but it was not found on the skin of healthy individuals. CONCLUSIONS: The Malassezia species composition in patients with PS differed from that of healthy individuals. M. restricta and M. globosa were the main Malassezia species in patients with PS.

Short-Term Western Diet Intake Promotes IL-23‒Mediated Skin and Joint Inflammation Accompanied by Changes to the Gut Microbiota in Mice.

We previously showed that exposure to a high-sugar and moderate-fat diet (i.e., Western diet [WD]) in mice induces appreciable skin inflammation and enhances the susceptibility to imiquimod-induced psoriasiform dermatitis, suggesting that dietary components may render the skin susceptible to psoriatic inflammation. In this study, utilizing an IL-23 minicircle-based model with features of both psoriasiform dermatitis and psoriatic arthritis, we showed that intake of WD for 10 weeks predisposed mice not only to skin but also to joint inflammation. Both WD-induced skin and joint injuries were associated with an expansion of IL-17A‒producing γδ T cells and increased expression of T helper type 17 cytokines. After IL-23 minicircle delivery, WD-fed mice had reduced microbial diversity and pronounced dysbiosis. Treatment with broad-spectrum antibiotics suppressed IL-23‒mediated skin and joint inflammation in the WD-fed mice. Strikingly, reduced skin and joint inflammation with a partial reversion of the gut microbiota were noted when mice switched from a WD to a standard diet after IL-23 minicircle delivery. These findings reveal that a short-term WD intake‒induced dysbiosis is accompanied by enhanced psoriasis-like skin and joint inflammation. Modifications toward a healthier dietary pattern should be considered in patients with psoriatic skin and/or joint disease.

Dysbiosis of Oral Microbiota Associated with Palmoplantar Pustulosis.

BACKGROUND: Dysbiosis of oral microbiota is implicated not only in oral inflammatory lesions, but also in a variety of extraoral diseases. The etiology of palmoplantar pustulosis (PPP) remains unclear; however, it has been suggested that chronic inflammation caused by periodontopathic bacterial infection may play a role. OBJECTIVES/METHODS: To determine whether patients with PPP have altered diversity and composition of oral microbiota, we conducted the 16S rDNA analysis using saliva samples collected from 21 outpatients with PPP and 10 healthy individuals. RESULTS: We found that the proportion of bacteria in the phylum Proteobacteria was significantly lower in PPP patients (p = 0.025). At the genus level, patients with PPP had a significantly lower abundance of Neisseria (p = 0.014), which best accounted for the observed decrease in Proteobacteria. We also identified multiple minor genera and species that were represented at a significantly higher level in the PPP group, several of which have been associated with periodontal diseases. CONCLUSION: Our results suggest a possible link between PPP and dysbiosis of oral microbiota, particularly the lower abundance of Neisseria, the most predominant genus of Proteobacteria in healthy oral microbiota. Probiotics that improves oral dysbiosis may be beneficial for patients with PPP as an adjunctive therapy.