COVID-19 exacerbates psoriasis progression through inducing IFN-αexpression

As a global public health issue that can cause systemic diseases,COVID-19 inflicts various harms on patients and impacts those with comorbidities.Psoriasis is primarily driven by a subset of T helper cells and the cytokines[1],and microbial infection is a predisposing factor in up to 45%of patients[2].Infection with SARS-CoV-2 may trigger the aggravation of psoriasis.Thus,we conducted a survey to explore the proportion of psoriasis patients who experienced exacerbation and relapse after SARS-CoV-2 infection and also performed a preliminary investigation into the mechanisms involved.One hundred and twenty-four psoriasis patients(79 males and 45 females)who contracted COVID-19 were followed up and provided detailed information.

Cytokine release syndrome triggered by programmed death 1 blockade(sintilimab)therapy in a psoriasis patient:A case report

BACKGROUND In recent years,immune checkpoint inhibitors(ICIs)have demonstrated remarkable efficacy across diverse malignancies.Notably,in patients with advanced gastric cancer,the use of programmed death 1(PD-1)blockade has significantly prolonged overall survival,marking a pivotal advancement comparable to the impact of Herceptin over the past two decades.While the therapeutic benefits of ICIs are evident,the increasing use of immunotherapy has led to an increase in immune-related adverse events.CASE SUMMARY This article presents the case of a patient with advanced gastric cancer and chronic plaque psoriasis.Following sintilimab therapy,the patient developed severe rashes accompanied by cytokine release syndrome(CRS).Fortunately,effective management was achieved through the administration of glucocorticoid,tocilizumab,and acitretin,which resulted in favorable outcomes.CONCLUSION Glucocorticoid and tocilizumab therapy was effective in managing CRS after PD-1 blockade therapy for gastric cancer in a patient with chronic plaque psoriasis.

Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB

Psoriasis is a chronic autoimmune disease featured by patches on the skin.It is caused by malfunction of immune cells and keratinocytes with inflammation as one of its key features.Apigenin(API)is a natural flavonoid with anti-inflammatory and immunoregulatory properties.Therefore,we speculated that API can ameliorate psoriasis,and determined its effect on the development of psoriasis by using imiquimod(IMQ)-induced psoriasis mouse model.Our results showed that API attenuated IMQ-induced phenotypic changes,such as erythema,scaling and epidermal thickening,and improved splenic hyperplasia.Abnormal differentiation of immune cells was restored in API-treated mice.Mechanistically,we revealed that API is a key regulator of signal transducer activator of transcription 3(STAT3).API regulated immune responses by reducing interleukin-23(IL-23)/STAT3/IL-17A axis.Moreover,it suppressed IMQ-caused cell hyperproliferation by inactivating STAT3 through regulation of extracellular signal-regulated kinase 1/2 and nuclear factor-κB(NF-κB)pathway.Furthermore,API reduced expression of inflammatory cytokines through inactivation of NF-κB.Taken together,our study demonstrates that API can ameliorate psoriasis and may be considered as a strategy for psoriasis treatment.

Causal effect of psoriasis on aortic valve stenosis:a two-sample Mendelian randomization study

Background Epidemiological studies have suggested a potential connection between psoriasis and an increased risk of aortic valve stenosis(AS),though the impact of psoriasis on AS progression remains uncertain.The study aims to investigate the causal relationship between psoriasis and AS using Mendelian randomization(MR)analysis,as well as to uncover potential mechanisms underlying this association.Methods A two-sample MR analysis was conducted using publicly available summary statistics from genome-wide association studies(GWAS)of psoriasis and AS.Cis-eQTL and significant genes were identified for each causal single-nucleotide polymorphisms(SNPs),followed by pathway enrichment and protein-protein interaction(PPI)analysis for functional evaluation.Hub genes were pinpointed by Cytospace.The transcriptional profile of AS population was acquired,and interconnected genes networks were clustered using Molecular Complex Detection(MCODE).Results Our results demonstrate a significant causal relationship between psoriasis and AS,with a genetic predisposition to psoriasis associated with a higher AS risk(odds ratio:1.46).Pathway and PPI analyses unveiled 15 hub genes,including HLA-C,HLA-B,ISG15,IFIT3,and MX2,along with immune-related pathways linking psoriasis and AS.Moreover,the transcriptional profiling of the AS database highlighted the significant involvement of adaptive immune cells in AS development.Notably,among the 15 hub genes,ISG15,MX2,OAS3,OASL,IFI6,and EPSTI1 exhibited higher expression in the AS population.Conclusion Our study provides compelling evidence supporting a causal relationship between psoriasis and AS.Furthermore,the identified hub genes and immune-related pathways may play an important role in the development of both diseases.

Coleus forskohlii shows anti-psoriatic activity in imiquimod-induced psoriasis rats

Objective:To evaluate anti-psoriatic activity of Coleus forskohlii in rats with imiquimod-induced psoriasis.Methods:Imiquimod was used to induce psoriasis in rats.Body weight,skin thickness,erythema,scaling,spleen weight,and histological alternations were measured to assess the effect of Coleus forskohlii.Furthermore,an emulgel formulation containing Coleus forskohlii 10%was prepared and characterized along with its ex vivo permeation studies.Results:The emulgel formulation containing Coleus forskohlii 10%had a pH of 5.40±0.36,with optimum spreadability of(31.67±2.08)g/(cm·s)and viscosity of(15966.67±1274.10)cps,and enhanced both the rate and the extent of drug permeation through psoriatic skin.In an ex vivo study,the quantity of drug permeated(19.18%),deposited(52.38%),and drug remaining in the donor compartments(28.31%)was satisfactory.Coleus forskohlii significantly alleviated imiquimod-induced psoriasis by increasing glutathione and superoxide dismutase activity,decreasing malondialdehyde and nitric oxide levels,and alleviating histological alternations in rat skin.Conclusions:Coleus forskohlii can alleviate imiquimod-induced psoriasis,which may be used as a therapeutic candidate for the treatment of psoriasis.

The Application Progress of Skin Imaging Technology in Psoriasis

Skin imaging technologies such as dermoscopy, high-frequency ultrasound, reflective confocal microscopy and optical coherence tomography are developing rapidly in clinical application. Skin imaging technology can improve clinical diagnosis rate, and its non-invasiveness and repeatability make it occupy an irreplaceable position in clinical diagnosis. With the “booming development” of medical technology, skin imaging technology can improve clinical diagnosis rate. Researchers have made significant advances in assisting clinical diagnosis, prediction, and treatment of disease. This article reviews the application and progress of skin imaging in the diagnosis of psoriasis.

Systemic Amyloidosis Secondary to Psoriasis: A Rare, Autoimmune and Genetically-Determined Disorder That Is Amenable to Treatment with Cyclosporin A—Cyclosporin A for Psoriasis-Induced Amyloidosis

Background: Systemic secondary amyloidosis (SSA) is associated with chronic inflammatory disorders and/or chronic infections. Patients and Methods: Over the past 10 years;a total of 21 patients, with long-term (17 months) and extensive psoriasis (P) with psoriasis area severity index (PASI) >29, were evaluated. Results: Two patients had nephrotic syndrome (proteinuria 3.9 and 3.6 g/day) and decrease creatinine clearance (46 and 62 ml/minute). Their renal biopsy revealed Congo-red (+) nodular glomerulosclerosis that lacked immune-deposits and resisted wash with K-permanganate wash indicating SSA. Three months subsequent to Cyclosporin A (CyA) therapy with 100 mg twice daily;psoriasis improved in all patients with decrease in (PASI) from 29.5 to 3.5 1. In the 2 patients with SSA;proteinuria decreased to 2.1 and 1.8 g/day and creatinine clearance improved to 51 and 69 ml/minute. Such improvement persisted up to 2 years of follow up and up to 78 months in patients with SSA. Conclusion: psoriasis-induced SSA is an autoimmune disease, with genetic predisposition that is amenable to CyA therapy.

Advances in the function of traditional medicine for vitiligo treatment

Vitiligo has a significant impact on a substantial number of individuals worldwide.Traditional Chinese medicine has a long history of serving as a therapeutic treatment for vitiligo.Nevertheless,given the increasing volume of research on the utilization of traditional Chinese medicine for vitiligo treatment,it is imperative to conduct a comprehensive review that elucidates the efficacy of Chinese traditional medicine and other active ingredients in the treatment of vitiligo.This paper presents a comprehensive overview of the clinical preparations used to treat vitiligo,while also highlighting the potential monomers and extracts derived from traditional Chinese medicine for vitiligo treatment.A thorough analysis of the pharmacological effects of traditional Chinese medicine on vitiligo treatment will provide valuable insights and reliable information for the development of new treatment strategies.

Moyamoya syndrome may result from psoriasis: Four case reports

BACKGROUND Moyamoya syndrome(MMS)is a group of diseases that involves more than one underlying disease and is accompanied by moyamoya vascular phenomena.Psoriasis is a chronic immune skin disease closely linked to high blood pressure and heart disease.However,psoriasis-related MMS has not been reported.CASE SUMMARY We collected data on patients with stroke due to MMS between January 2017 and December 2019 and identified four cases of psoriasis.Case histories,imaging,and hematological data were collected.The average age of the initial stroke onset was 58.25±11.52 years;three cases of hemorrhagic and one case of ischemic stroke were included.The average duration from psoriasis confirmation to the initial MMS-mediated stroke onset was 17±3.56 years.All MMS-related stenoses involved the bilateral cerebral arteries:Suzuki grade III in one case,grade IV in two cases,and grade V in one case.Abnormally elevated plasma interleukin-6 levels were observed in four patients.Two patients had abnormally elevated immunoglobulin E levels,and two had thrombocytosis.All four patients received medication instead of surgery.With an average follow-up time of 2 years,two causing transient ischemic attacks occurred in two patients,and no hemorrhagic events occurred.CONCLUSION Psoriasis may be a potential risk factor for MMS.Patients with psoriasis should be screened for MMS when they present with neurological symptoms.

Toll-like receptors 2 polymorphism is associated with psoriasis: A case-control study in the northern Chinese population

Background:Psoriasis is a disease caused by genetics and immune system dysfunction,affecting the skin and joints.Toll-like receptors(TLRs)play an important role in triggering the innate immune response and controlling adaptive immunity.The role of TLR2 in the progression of psoriasis is not well understood.Methods:A case-control study was conducted on a northern Chinese Han population,consisting of psoriasis patients and healthy control subjects.Genotyping was performed using the tetra-primer amplification refractory mutation system-polymerase chain reaction(ARMS-PCR),and allele and genotype frequencies of four SNPs in TLR2 were analyzed in 270 psoriasis patients and 246 healthy controls.Results:Four TLR2 SNPs(rs11938228,rs4696480,rs3804099,rs5743699)were genotyped and found to be in linkage disequilibrium.The genotype distributions of rs11938228 and rs4696480 in two groups were in Hardy-Weinberg equilibrium and statistically significant except for the overdominance model.The haplotypes ATTC and ATCC were found to be protective against psoriasis.Conclusion:Our study found a correlation between TLR2 genetic variations and the likelihood of psoriasis in northern China.

Secoemestrin C Ameliorates Psoriasis-like Skin Inflammation in Mice by Suppressing the TNF-α/NF-κB Signaling Pathway

Objective Secoemestrin C(SC),an epitetrathiodioxopiperazine isolated from Aspergillus nidulans,has been previously reported to have immunomodulatory and hepatoprotective effects against acute autoimmune hepatitis.However,the effect of SC on regulating the inflammation and its underlying mechanisms in the pathogenesis of psoriasis remain unclear.This study aimed to evaluate the effects of SC on inflammatory dermatosis both in vitro and in vivo.Methods In vitro,HaCaT cells were induced with tumor necrosis factor-alpha(TNF-α,10 ng/mL)to establish an inflammatory injury model,and the expression of nuclear transcription factor-κB(NF-κB)pathway components was measured using qRT-PCR and Western blotting.An in vivo mouse model of imiquimod(IMQ)-induced psoriasis-like skin inflammation was used to evaluate the effectiveness of SC in alleviating psoriasis.Results SC significantly blocked the activation of NF-κB signaling in TNF-α-stimulated HaCaT cells.In addition,systemic and local administration of SC improved psoriatic dermatitis in the IMQ-induced mouse model.SC reduced skin scale and significantly inhibited the secretion of inflammatory factors in skin lesions.Conclusion The protective effect of SC against psoriatic-associated inflammation reveals its potential therapeutic value for treating psoriasis.

Medical dilemma:Programmed death 1 blockade(sintilimab)therapy in patients suffering from tumours combined with psoriasis

Tumour immunotherapy represented by immune checkpoint inhibitors(ICIs)has greatly improved the overall prognosis of patients with malignant tumours,and is regarded as an important breakthrough in the field of medicine in recent years.ICIs have gradually become the core of tumour therapy and are increasingly used in the clinic.In order to achieve early clinical prediction and management of immune-related adverse events(irAEs),it is still necessary to perform further research on the mechanisms,risk factors,and predictors of irAE occurrence in the future.Zhou et al describe the consultation of a patient with advanced gastric cancer combined with chronic plaque psoriasis.This case provides an important reference for the use of programmed cell death protein-1(PD-1)inhibitors in patients of tumours combined with chronic plaque psoriasis.This case also highlights that screening of high-risk groups for irAEs is critical before applying PD-1 inhibitors to patients with chronic psoriasis combined with tumours.PD-1 inhibitors are new and potent antineoplastic agents that can cause serious immunerelated adverse events such as toxic epidermal necrolysis release and psoriasis.Glucocorticosteroids are the first-line agents for irAEs.The incidence of rheumatic irAEs may be higher in reality,which will inevitably become a new challenge for rheumatologists and dermatologists.

Cytokine release syndrome induced by anti-programmed death-1 treatment in a psoriasis patient:A dark side of immune checkpoint inhibitors

In recent years,cancer immunotherapy has introduced novel treatments,such as monoclonal antibodies,which have facilitated targeted therapies against tumor cells.Programmed death-1(PD-1)is an immune checkpoint expressed in T cells that regulates the immune system’s activity to prevent over-activation and tissue damage caused by inflammation.However,PD-1 is also expressed in tumor cells and functions as an immune evasion mechanism,making it a therapeutic target to enhance the immune response and eliminate tumor cells.Consequently,immune checkpoint inhibitors(ICIs)have emerged as an option for certain tumor types.Nevertheless,blocking immune checkpoints can lead to immune-related adverse events(irAEs),such as psoriasis and cytokine release syndrome(CRS),as exemp-lified in the clinical case presented by Zhou et al involving a patient with adva-nced gastric cancer who received sintilimab,a monoclonal antibody targeting PD-1.Subsequently,the patient experienced exacerbation of psoriasis and CRS.The objective of this editorial article is to elucidate potential immunologic mechanisms that may contribute to the development of CRS and psoriasis in patients receiving ICIs.It is crucial to acknowledge that while ICIs offer superior safety and efficacy compared to conventional therapies,they can also manifest irAEs affecting the skin,gastrointestinal tract,or respiratory system.In severe cases,these irAEs can lead to life-threatening complications such as circulatory shock or multiorgan failure.Consequently,it is recommended that patients receiving ICIs undergo regular monitoring to identify and manage these adverse events effectively.

Mechanism of traditional Chinese medicine in the treatment of psoriasis with depression:A review

Psoriasis is a kind of immune-mediated, chronic, inflammatory skin disease, which is often associated with different degrees of psychological disorders. Specifically, there is a significant correlation between psoriasis and depression, and they show the relationships of reciprocal causation and mutual promotion. Psoriasis with depression is more harmful than simple psoriasis, and its prognosis is worse, which brings a huge burden to the family and society and is worthy of clinical attention. Based on the pathogenic factors of western medicine and pathogenesis of traditional Chinese medicine in psoriasis with depression, the paper summarized and elaborated the research progress on the mechanism of traditional Chinese medicine in the treatment of psoriasis with depression, in order to provide new ideas for clinical treatment.

二甲双胍通过NLRP3炎症小体通路对皮肤角质形成细胞增殖和凋亡的双向调节研究

背景扁平苔藓是一种皮肤-黏膜慢性炎症性疾病。因其病因不明,许多患者治疗效果欠佳,严重影响生活质量,有必要深入研究扁平苔藓的发病机制,为其药物筛选提供新靶点。目的探讨二甲双胍通过NLRP3炎症小体通路对皮肤角质形成细胞增殖和凋亡的调控作用。方法实验时间为2020—2023年。体外实验以人永生化角质形成细胞株HaCaT为研究对象,分为4组:对照组、脂多糖(LPS)组(5μg/mL)、二甲双胍组(Met组:10 mmol/L)、LPS与二甲双胍联合组(LPS+Met组:LPS 5μg/mL刺激2 h后,再给予二甲双胍10 mmol/L处理)。体内实验以BALB/c小鼠为研究对象,利用咪喹莫特涂抹小鼠背部皮肤诱导了银屑病样皮炎模型,并制备了二甲双胍乳膏进行治疗,将小鼠随机分为3组:对照组、咪喹莫特组(IMQ组)、咪喹莫特与二甲双胍联合组(IMQ+Met组),每组10只;对照组小鼠于背部涂抹凡士林,IMQ组小鼠于背部涂抹咪喹莫特软膏,IMQ+Met组小鼠于背部涂抹IMQ软膏12 h后再涂抹二甲双胍乳膏;1次/d,连续7 d。采用细胞增殖试剂盒(CCK-8)和流式细胞术检测二甲双胍对HaCaT细胞增殖和凋亡的影响;采用Western Blotting、酶联免疫吸附实验(ELISA)和半胱氨酸天冬氨酸蛋白酶1(Caspase-1)活性实验检测二甲双胍处理HaCaT细胞后NOD样受体蛋白3(NLRP3)炎症小体通路的蛋白表达情况及活性水平;最后采用皮肤组织切片苏木素-伊红(HE)染色和免疫组化检测二甲双胍对咪喹莫特诱导银屑病小鼠皮炎的抗炎效果。结果CCK-8实验结果显示:LPS组、Met组、LPS+Met组HaCaT细胞48 h存活率均低于对照组,而LPS+Met组HaCaT细胞48 h存活率高于LPS组(P<0.05)。流式细胞术结果显示:LPS组、Met组HaCaT细胞48 h G2/M期细胞、细胞凋亡比例均高于对照组,而LPS+Met组HaCaT细胞48 h G2/M期细胞、细胞凋亡比例低于LPS组(P<0.05)。Western Blotting结果显示:LPS组、Met组HaCaT细胞NLRP3炎症小体通路Caspase-1 p40、Caspase-1 p20、白介素(IL)-1β、IL-18蛋白表达均高于对照组,而LPS+Met组HaCaT细胞NLRP3炎症小体通路Caspase-1 p40、Caspase-1 p20、IL-1β、IL-18蛋白表达低于LPS组(P<0.05)。ELISA实验结果显示:LPS组、Met组HaCaT细胞NLRP3炎症小体通路IL-1β、IL-18水平、Caspase-1相对活性均高于对照组,而LPS+Met组HaCaT细胞NLRP3炎症小体通路IL-1β、IL-18水平、Caspase-1相对活性低于LPS组(P<0.05)。皮肤组织切片HE染色显示:IMQ+Met组小鼠二甲双胍涂抹明显改善了咪喹莫特对皮肤的损害。免疫组化结果显示:IMQ+Met组小鼠则显著降低了NLRP3、Caspase-1、IL-1β和IL-18的表达。结论二甲双胍通过NLRP3炎症小体通路双向调节皮肤角质形成细胞的增殖和凋亡,并能够改善咪喹莫特诱导的银屑病样小鼠的皮肤损害,有望为二甲双胍临床上用于治疗扁平苔藓提供理论依据。

佩索利单抗治疗急性泛发性脓疱型银屑病二例并文献复习

报道佩索利单抗治疗2例急性泛发性脓疱型银屑病(GPP)的疗效。2例患者均为男性,均有寻常型银屑病病史,均治疗1次(900 mg)。治疗前24 h的GPP医师总体评估(GPPGA)脓疱评分均为4,GPP皮损面积和严重程度指数(GPPASI)评分分别为48.0和59.3。2例患者治疗后48 h GPPGA脓疱单项评分均0,GPPASI评分改善率为91.04%和89.21%。治疗过程中,2例患者的实验室指标如白细胞计数、中性粒细胞计数及比例、C反应蛋白均在应用佩索利单抗后48 h内逐步回归或接近正常水平,且观察1周无反复,体温在给药后24 h内恢复正常且无反复。

银屑病相关miRNA的研究进展

微RNA(miRNA)可通过改变靶信使RNA的翻译或稳定性在RNA沉默和转录后基因表达调控中发挥作用。此外,miRNA也是细胞生长、分化、凋亡、免疫反应等细胞过程的重要调节因子。miRNA可调节银屑病角质形成细胞的分化、增殖、凋亡和T细胞的激活、生存以及免疫细胞与角蛋白细胞之间的干扰,不同的miRNA及其靶基因可通过不同的信号转导通路参与银屑病的发生发展。银屑病中高表达的miRNA主要包括miR-31、miR-21、miR-203、miR-146a等,低表达的miRNA主要包括miR-125b、miR-205-5p等。因此,全面了解银屑病中异常表达的miRNA可以为阐明疾病的发病机制、寻找相关诊断标志物提供坚实的理论基础,同时也可为银屑病的临床治疗提供新思路。

白细胞介素-17C在自身免疫性皮肤病中的研究进展

白细胞介素17家族(interleukin-17s,IL-17s)具有促炎效应,参与各种自身免疫性疾病的发生发展。IL-17C是IL-17细胞因子家族中的重要成员之一,不同于广泛来源于各种免疫细胞的IL-17A,IL-17C主要由上皮细胞分泌并通过IL-17RE/A受体复合物发挥作用,在银屑病、特应性皮炎等自身免疫性皮肤病中均存在表达异常。本文综述了IL-17C与自身免疫性皮肤病之间关系的研究进展。

近5年油腻型头皮脂溢性皮炎的研究进展

脂溢性皮炎是发生在皮脂腺丰富部位的慢性、复发性、炎症性皮肤病,多发于头面部,若发于头部则称为“头皮脂溢性皮炎”。油腻型头皮脂溢性皮炎以头发油腻多脂、瘙痒起白屑为主要特征,因此临床见头发油腻兼其他症状者,可参照此病论治。头发油腻发亮极大程度地影响了人们的外在形象,故此病的治疗受到了广泛的关注。文章整理近5年油腻型头皮脂溢性皮炎治疗的相关文献,从现代医学、中医学、中西医结合以及日常清洁控油护理的角度,总结其研究进展。

Highlights in pathogenesis of vitiligo

Vitiligo is a common pigmentary disorder. Many studies across decades and all over the world have attempted to illustrate the pathogenesis behind it; however, the pathogenesis of vitiligo remains elusive. This review article, we present the findings behind the most and updated theories behind this psychologically debilitating and disfiguring disease. The discussion begun with the role of genetic predisposition followed by neural theory first proposed in the 1950 s. Wehighlight the autoimmune hypothesis, followed by the reactive oxygen species model, zinc-α2-glycoprotein deficiency hypothesis, viral theory, intrinsic theory and biochemical, molecular and cellular alterations accounting for loss of functioning melanocytes in vitiligo. Many theories were elaborated to clarify vitiligo pathogenesis. It is a multifactorial disease involving the interplay of several factors. Future research is needed to clarify the interaction of these factors for better understanding of vitiligo pathogenesis and subsequent successful treatment.