Yanping Bai

Background/Objectives: Chronic pruritus of unknown origin (CPUO) is mechanistically poorly resolved, and its relationship to atopic dermatitis (AD) is unclear. We asked how much apparent separation survives removal of leakage. Methods: Public bulk skin data (GSE237920; four healthy, four AD, four CPUO) were analyzed by differential expression and an XOmiVAE-inspired latent model, with public single-cell and atlas resources for context. Every label-dependent step was then re-executed inside each cross-validation fold, with label permutation and 1000 bootstraps. A frozen composite niche score was applied unchanged to prurigo nodularis (GSE210854) and AD (GSE174582) cohorts. Results: Fully nested, the latent classifier separated CPUO from healthy skin (AUC 1.000; permutation p = 0.020) but not from AD (0.741; p = 0.140); randomized labels also reached 1.00. The composite score reached 0.919 against healthy skin but did not exceed its null (p = 0.086). Six genes recurred in ≥80% of bootstraps, five within the signature. Cell-type-restricted blood analysis recovered CPUO-associated monocyte CCL3 upregulation. In both validation cohorts, the frozen score was reduced, not elevated, in lesional skin. Conclusions: CPUO skin differs from healthy skin and occupies the low-inflammatory, epidermal-stress-dominated pole opposite lesional inflammatory skin, but cannot be robustly separated from AD at twelve samples.

Objective: To systematically analyze the research landscape, knowledge structure, and evolution hotspots in macrophages and psoriasis research over the past decade through bibliometric analysis, providing guidance for mechanistic investigation and therapeutic strategies. Methods: Literature published between January 2015 and December 2024 was retrieved from the Web of Science database and Scopus. The softwares CiteSpace, VOSviewer, Scimago Graphica, and Excel were employed for bibliometric analysis, including co-occurrence networks, clustering analysis, and keyword evolution analysis. Results: A total of 2012 articles were identified from 2015 to 2024, showing an upward trend first and then slightly decreased. China and the United States were the leading contributors, while international collaboration formed four major clusters. Core journals such as Frontiers in Immunology and Journal of Immunology played pivotal roles in knowledge dissemination. Research hotspots evolved from fundamental inflammatory mechanisms to targeted biologic therapies, highlighting a growing emphasis on precision medicine and the immunopathogenesis of psoriasis. Conclusion: Macrophage and psoriasis-related research represents a rapidly evolving interdisciplinary field transitioning from isolated pathological studies to comprehensive research integrating advanced technologies with clinical applications. While substantial progress has been achieved in exploring macrophage roles in psoriasis pathogenesis, significant gaps remain between laboratory discoveries and clinical translation. Future research should prioritize international collaboration, application studies, and precision therapeutic strategies targeting macrophage-mediated pathways.

Background: Psoriasis is a chronic inflammatory skin disease involving dysregulated immune responses and complex genetic factors. This study combines single-cell RNA sequencing (scRNA-seq), gene expression profiling, and genetic analysis to explore cellular and molecular contributors to psoriasis. Methods: Single-cell RNA-seq data (n = 3 psoriasis, n = 2 control; GSE228421) were used for cell-type annotation and functional characterization. T cell subsets were analyzed for differentiation trajectories and cell-cell communication. Differentially expressed genes in mucosal-associated invariant T (MAIT) cells were evaluated by enrichment analysis. Candidate gene causality was tested via eQTL-based Mendelian randomization (MR) and supported by bulk RNA-seq validation. Results: MAIT cells were enriched in psoriatic lesions and exhibited strong intercellular interactions. Functional analyses revealed activation of IL6-JAK-STAT3 signaling, TNF-NFκB pathway, and glycolysis in MAIT cells. MR identified RPS20 as a protective factor (OR = 0.5994, p = 0.011) and PFN1 as a potential risk gene (OR = 1.7229, p = 0.037), with PFN1 highly expressed in MAIT cells. Colocalization analysis showed no significant genetic overlap between PFN1 expression and psoriasis risk. Metabolic profiling revealed differential pathway involvement in PFN1+ and PFN1− MAIT cells. Conclusion: Our integrative analysis highlights MAIT cells and PFN1 as likely contributors to psoriasis pathogenesis. These findings offer insights into immune and metabolic alterations, suggesting potential targets for therapeutic intervention.

Background: Psoriasis is a common chronic inflammatory skin disease with a complex pathogenesis. Recently, the role of gut microbiota in psoriasis has attracted increasing attention. A systematic bibliometric analysis of relevant literature is necessary to understand better the current state and development trends in this field.Materials and methods: The Web of Science Core Collection database was searched for literature indexed from 2004 to October 15, 2024. Bibliometric analysis was conducted using Bibliometrix, CiteSpace (version 6.3.R1), R 4.2.2 with the Bibliometrix package, Scimago Graphica 1.0.45, and VOSviewer (version 1.6.20.0) to visualize publication types, years, authors, countries, institutions, journal sources, references, and keywords.Results: The development of psoriasis and gut microbiota research can be divided into two phases: slow growth (2004–2014) and rapid development (2014–2024). Lidia Rudnicka is the most active and influential author. China produced the highest number of publications, followed by the United States, which had the highest number of citations per article. The International Journal of Molecular Sciences published the most articles. In contrast, articles in the Journal of Investigative Dermatology, British Journal of Dermatology, and Journal of Allergy and Clinical Immunology were cited over 1,000 times. Keyword and co-citation analyses identified evolving research hotspots. Early studies focused on the association between gut microbiota and comorbid inflammatory diseases. Recent research has delved into specific mechanisms, such as disruption of gut barrier function, short-chain fatty acid metabolism alterations, impaired regulatory T-cell function, and excessive activation of Th17 cells. These mechanisms highlight how gut dysbiosis exacerbates psoriasis patients’ systemic inflammation and skin lesions.Conclusion: The field of psoriasis and gut microbiota research is developing rapidly despite uneven research distribution. This bibliometric evaluation assesses the current state of research and provides new perspectives for understanding the complex interactions between microbes and the host. Future efforts should strengthen international collaboration to deeply explore the mechanisms of gut microbiota’s role in psoriasis, especially its potential applications in disease diagnosis and treatment.

Introduction: Generalized pustular psoriasis (GPP) and bullous pemphigoid (BP) are two distinct but occasionally coexisting inflammatory skin disorders. Their simultaneous presence presents diagnostic and therapeutic challenges. Spesolimab and dupilumab are novel biologics targeting the IL-36 and IL-4/IL-13 pathways, respectively. However, their sequential use in treating GPP with BP has not been previously reported. Case Presentation: We report a 58-year-old man with a 10-year history of psoriasis who developed acute GPP followed by BP. Initial acitretin therapy resolved pustules but not bullae. A single dose of intravenous spesolimab led to rapid improvement of systemic symptoms and pustular lesions. Persistent bullae were subsequently treated with dupilumab (600 mg loading dose, then 300 mg biweekly), resulting in complete resolution within 2 months. The patient remained relapse-free for 6 months, with no adverse events. Conclusion: This case highlights the potential of sequential spesolimab and dupilumab therapy as an effective and safe approach for managing GPP coexisting with BP. Targeting distinct inflammatory pathways may provide a new treatment option for complex dermatological comorbidities.

Introduction: Generalized pustular psoriasis (GPP) is a rare and potentially life-threatening auto-inflammatory disease. Currently, there are no consensus-based guidelines or universally accepted treatments. Biologics represent a potential therapeutic option. This study systematically assessed the efficacy and safety of biologics in GPP.Methods: Relevant studies from three databases were systematically searched until June 28, 2024. Statistical information, including the single-arm proportion rate of the outcomes and 95% confidence intervals (CIs), was analyzed to determine treatment effects. Heterogeneity was assessed using I² values, and subgroup analyses were performed based on drug targets and treatment durations. Data were quantitatively synthesized using a random-effects meta-analysis. Analyses were performed using R statistical software version 4.4.0.Results: A total of 329 patients from 16 studies were included. The proportion of responders treated with IL-36 inhibitors and IL-17 inhibitors is higher than those treated with TNF-α inhibitors and IL-23 inhibitors. IL-36 inhibitors appear to achieve the highest response rates between 4 and 8 weeks, while IL-17 inhibitors, TNF-alpha inhibitors, and IL-23 inhibitors show a gradual increase in response rates up to 12 weeks. IL-36 inhibitors achieve a 40% (95% CI: 27%-54%) GPPASI75 response rate and a 55% (95% CI: 41%-68%) GPPGA (0,1) response rate within 2 weeks, significantly outperforming other biologics. The recurrence rates of GPP within 52 weeks, ranked from highest to lowest, are: IL-36 inhibitors (21% [95% CI: 9%-28%]), TNF-alpha inhibitors (20% [95% CI: 2%-46%]), IL-17 inhibitors (15% [95% CI: 1%-37%]), and IL-23 inhibitors (5% [95% CI: 0%-29%]). Additionally, 6% (95% CI: 1%-11%) of patients experienced severe adverse events.Discussion: This meta-analysis highlights the efficacy and safety of biologics in patients with GPP, offering valuable evidence to guide future clinical practice. IL-36 inhibitors show a faster and more substantial clinical response in GPP compared to other biologics. Further research is necessary to assess their role in specific subpopulations and to evaluate their potential long-term effects on flare prevention.

Rare cases of arsenical keratosis are attributed to the ingestion of arsenic-containing traditional Chinese medicines for conditions such as psoriasis. Arsenic is a potent carcinogen, and squamous cell carcinoma is known to develop in arsenical keratosis. A 51-year-old male patient with a 30-year history of psoriasis and a history of arsenic poisoning presented with suppuration, ulceration, and pain one and a half years after trauma to the right thumb. These symptoms had recurred after wound debridement, lesion resection, and pedicle flap transplantation. Histopathological examination of the skin lesions had suggested squamous cell carcinoma, and subsequent PET-CT examination had shown proliferation and enlargement of lymph nodes. Following right forearm amputation and radiofrequency ablation, additional lumps had been observed, but the patient had declined further surgery. Physical examination showed palpable enlarged axillary lymph nodes, which was confirmed by ultrasound. After three cycles of first-line immunotherapy with toripalimab combined with albumin paclitaxel and cisplatin chemotherapy, masses in the right upper arm were reduced. This case highlights the risks of arsenic-containing medicines used for treating psoriasis. Attention should be paid to the use of standardized treatments in psoriasis, as well as the probability of malignant transformation in arsenical keratosis.

Background: The risk of asthma in patients with psoriasis has been identified in previous studies, but the bidirectional association between the two has not been fully explored. Methods: We thoroughly searched PubMed, Embase, and the Cochrane Library to find relevant observational studies published from the inception of these databases to October 2023. All the risk and bias assessments were analyzed by STATA 16.0. Where the heterogeneity was less than 50%, the fixed effect model was utilized. While where the level of heterogeneity was more than 50%, the random effect model was applied. Moreover, to identify publication bias, a visual funnel chart, and Egger’s test were applied. Results: A total of 12,396,911 participants from 16 studies, published between 2011 and 2023 were included in this meta-analysis. We found that psoriasis patients had a higher risk of developing asthma (OR = 1.48, 95%CI 1.28–1.68). Meanwhile, asthma patients also had a higher overall risk of developing psoriasis (OR = 1.33, 95%CI 1.23–1.44). In the subgroup analysis, we found that the type of study, age, and severity of the psoriasis were significant factors in the survey of asthma risk in psoriasis patients. Conclusions: In the present systematic review and meta-analysis, we found a bidirectional association between psoriasis and asthma with significantly increased risk. As a result, clinicians should make patients aware of the connection between the two, particularly adolescents or patients with moderate to severe psoriasis who need to be informed about the rising likelihood of developing asthma. Trial registration: Registration number CRD42023390111.

Background Psoriasis is a common, chronic, inflammatory papulosquamous skin disease which is difficult to be cured. Qingre Liangxue Decoction(QRLXD), originated from the classic formula Xijiao Dihuang Decoction, as a famous classical prescription for the treatment of psoriasis vulgaris (PV) with blood-heat syndrome in the traditional Chinese medicine (TCM), shows good efficacy in clinical practice. Since the mechanism of action is still unclear, this article was aimed to profile the absorbed prototype constituents in rat serum after its oral administration and explore the molecular mechanism of QRLXD using network pharmacology and molecular docking technology. Methods First, chemical components of QRLXD absorbed in vivo were comprehensively analyzed by Ultra high performance liquid chromatography-high resolution mass spectrometry (UPLC-Q-Exactive-Orbitrap-MS) method. The Swiss Target Prediction was used to predict corresponding potential target genes of active compounds. Simultaneously, 5 disease databases were used to search and filter psoriasis vulgaris (PV) with blood-heat syndrome targets, and then we constructed a protein-protein interaction (PPI) network. Metascape were utilized for GO and KEGG enrichment analysis. After that, we constructed a network of "QRLXD-compounds-target-pathway-PV" by Cytoscape. Molecular docking simulation was conducted to further refine the drug-target interaction by AutoDock software. Results A total of 68 ingredients were identified in vitro and 18 ingredients in vivo, targeting 523 proteins, among which 129 were related to psoriasis. The protein with a higher degree in the PPI network is TNF, ALB, AKT1, STAT3 and EGFR. 1488 GO biological process items and 162 KEGG signal pathways were enriched. GO and KEGG indicated that QRLXD treatment of psoriasis mainly involves protein kinase activity, protein tyrosine kinase activity, phosphotransferase activity, alcohol group as acceptor and other biological processes.The signaling pathways mainly include the pathways in cancer,PI3K-Akt ,MAPK and IL-17 signaling pathways. The main compounds and the target protein had a good binding ability in molecular docking. The molecular docking results revealed that Dibutyl phthalate, Ethyl benzoylformate, Scopoletin, Albiflorin R1, 3-Hydroxycoumarin have higher affinity with TNF, ALB and AKT1. Conclusion This study suggests that QRLXD against PV with blood-heat syndrome through multiple components, multiple targets and multiple pathways. This study identified effective compounds of QRLXD in vivo and predicted potential molecular mechanisms of QRLXD in psoriasis treatment, serving as an important basis for the modernization of QRLXD.