• liver diseases
• meta-analysis
• non-alcoholic fatty liver disease
• psoriasis

• Amygdalin
• Inflammation
• Psoriasis
• Skin barrier dysfunction
• Tape stripping

• Psoriasis/drug therapy
• Psoriasis/pathology
• Psoriasis/chemically induced
• Amygdalin/pharmacology
• Animals
• Humans
• Filaggrin Proteins
• Mice
• Disease Models, Animal
• Imiquimod
• Keratinocytes/drug effects
• Keratinocytes/metabolism
• Male
• HaCaT Cells
• Skin/pathology
• Skin/drug effects
• Skin/metabolism
• Mice, Inbred BALB C
• Cytokines/metabolism

• 82374313 National Natural Science Foundation of China

• Air pollution
• Skin diseases
• Smoke

• Humans
• Air Pollutants/toxicity
• Air Pollution
• Oxidative Stress/drug effects
• Particulate Matter/toxicity
• Polycyclic Aromatic Hydrocarbons/toxicity
• Skin/drug effects
• Skin Diseases/chemically induced
• Volatile Organic Compounds/toxicity

• CDK8 inhibitor
• Design
• Psoriasis activity
• Pyrrolo-pyridine

• Animals
• Cyclin-Dependent Kinase 8/antagonists & inhibitors
• Cyclin-Dependent Kinase 8/metabolism
• Psoriasis/drug therapy
• Humans
• Protein Kinase Inhibitors/pharmacology
• Protein Kinase Inhibitors/chemistry
• Mice
• NF-kappa B/metabolism
• NF-kappa B/antagonists & inhibitors
• Pyridines/pharmacology
• Pyridines/chemistry
• Mice, Inbred BALB C
• Interleukin-10/metabolism
• Male
• Pyrroles/pharmacology
• Pyrroles/chemistry
• Forkhead Transcription Factors/metabolism
• Drug Discovery/methods
• Tumor Necrosis Factor-alpha/metabolism
• Tumor Necrosis Factor-alpha/antagonists & inhibitors
• Disease Models, Animal
• Skin/drug effects
• Skin/pathology
• Skin/metabolism

• IFN
• Immunity
• Psoriasis
• Skin
• Therapy

• HaCaT
• NF-κB
• PIAS3
• STAT3
• psoriasis

• 81602753 National Natural Science Foundation of China
• 2020T130159 China Postdoctoral Science Foundation

• HMGB1 signaling pathway
• HaCaT cells
• etanercept
• inflammation
• psoriasis

• Animals
• Mice
• Disease Models, Animal
• Etanercept
• HMGB1 Protein/metabolism
• HMGB1 Protein/pharmacology
• HMGB1 Protein/therapeutic use
• Imiquimod
• Inflammation/chemically induced
• Inflammation/drug therapy
• Inflammation/pathology
• Keratinocytes/metabolism
• Lipopolysaccharides/metabolism
• Psoriasis/chemically induced
• Psoriasis/drug therapy
• Receptor for Advanced Glycation End Products/metabolism
• Receptor for Advanced Glycation End Products/therapeutic use

• cancer
• codelivery
• combination therapy
• inflammatory bowel disease
• lipid nanoparticles
• psoriasis

• Humans
• Nanoparticles
• Neoplasms/drug therapy
• Drug Delivery Systems
• Lipids

• P30 GM127200 NIGMS NIH HHS
• R01 AA027695 NIAAA NIH HHS
• R01 CA235863 NCI NIH HHS
• R01 DK120533 NIDDK NIH HHS
• NIH

• 3D-SeboSkin
• NFκB
• SZ95 sebaceous gland cell line
• adalimumab
• autophagy
• cytokines
• ex vivo
• hidradenitis suppurativa
• proteins

• Antibodies, Anti-Idiotypic/therapeutic use
• Antibodies, Monoclonal, Humanized/therapeutic use
• Autoantibodies
• Biological Products/therapeutic use
• Cytokines
• Humans
• Interleukin-17
• Interleukin-8
• Psoriasis/drug therapy

• Anti-Inflammation
• Antiviral
• Chinese Woad
• Complementary Medicine
• Ethnopharmacology
• Isatis indigotica Fortune

• Inflammation
• NB-UVB
• UVB irradiation
• chronic skin disease
• gene
• high-throughput RNA-sequencing
• inflammation
• pathogenesis
• psoriasis
• translational study

The V-domain Ig Suppressor of T-cell Activation (VISTA) is an immune checkpoint regulator that suppresses immune responses and is readily expressed on human and murine myeloid cells and T cells. This immunosuppressive pathway can be activated using VISTA agonists. Here, we report the development of murine anti-human VISTA (anti-hVISTA) monoclonal antibodies (mAbs), anti-hVISTA nanobodies (Nbs), and cross-reactive rat anti-murine/human VISTA (anti-hmVISTA) mAbs. All mAbs and Nbs generated bound to VISTA (human and/or murine) with dissociation constants in the sub-nanomolar or low nanomolar range. Competition analysis revealed that the selected Nbs bound the same or a nearby epitope(s) as the human VISTA-specific mAbs. However, the cross-reactive mAbs only partially competed with Nbs for binding to hVISTA. All mAbs and one Nb (hVISTANb7) were able to strongly detect VISTA expression on primary human monocytes. Importantly, the murine anti-hVISTA mAbs 7E12 and 7G5 displayed strong agonistic activity in human peripheral blood mononuclear cell cultures, while Nb7 and rat anti-hmVISTA mAbs 3C3, 7C6, 7C7, and 7G1 also behaved as hVISTA agonists, albeit to a lesser extent. Cross-reactive mAbs 7C7 and 7G1 further displayed agonistic potential in murine splenocyte assays. Importantly, mAb 7G1 significantly reduced inflammation associated with the murine model of imiquimod-induced psoriasis. These agonistic VISTA mAbs may represent therapeutic leads to treat inflammatory disorders.

• ConA
• VISTA
• agonistic
• anti-inflammatory
• monoclonal antibodies
• nanobodies
• psoriasis

• Chemokine CCL5
• Crocus/chemistry
• Cytokines/metabolism
• Gene Expression/drug effects
• HaCaT Cells
• Humans
• Interferon-gamma
• Molecular Structure
• Phytochemicals/isolation & purification
• Phytochemicals/pharmacology
• Saponins/isolation & purification
• Saponins/pharmacology
• Tumor Necrosis Factor-alpha

• Comorbidities
• Epidemiology
• Genetics
• Immunopathogenesis
• Inflammation
• Psoriasis

Psoriasis, affecting approximately 2% of the worldwide population, is a chronic, inflammatory skin disease in which overexpression of proinflammatory cytokines is observed. Most of the available data on the influence of antipsoriatic therapy on the cytokine serum concentration are inconsistent and based on short-term observations.

To evaluate the influence of long-term biologic therapy with tumor necrosis factor α (TNF-α) blockers (adalimumab, etanercept, infliximab) and IL-12/23 inhibitor (ustekinumab) on the level of IL-6, IL-22 in the sera of patients with psoriasis.

Blood samples were collected from 42 psoriatic patients in order to determine IL-6 and IL-22 serum concentrations prior to and at the 3^rd, 12^th, 24^th and 36^th month of biologic therapy. Psoriasis Activity and Severity Index (PASI) was assessed at the same time points. The control group consisted of 30 sex- and age-matched healthy volunteers.

Mean PASI index at baseline was 14.49 ±3.69 and decreased significantly until the end of the observation. Mean IL-6 serum concentration decreased significantly in all study groups (p < 0.05). A statistically significant decrease in IL-22 concentrations was demonstrated during the treatment with adalimumab and infliximab but not etanercept or ustekinumab.

According to obtained results, IL-6 and IL-22 serum concentration may be an accurate marker of response to antipsoriatic therapy, even though not correlated with PASI index. Biologic therapy in psoriasis allows for long-term clinical improvement expressed not only by the remission of skin lesions, but also by lowering serum concentrations of pro-inflammatory interleukins.

• biologic therapy
• interleukin 22
• interleukin 6
• psoriasis

• IL6R
• PAR-CLIP
• keratinocytes
• miR-197
• psoriasis

• Drug-provoked psoriasis
• Environmental factors
• Inflammatory skin disease
• Psoriasis risk factors

Many autoimmune disorders such as psoriasis lead to the alteration of skin components which generally manifests as unwanted topical symptoms. One of the most widely approved psoriasis-like animal models is the imiquimod (IMQ)-induced mouse model. This representation mimics various aspects of the complex cutaneous pathology and could be appropriate for testing topical treatment options. We perform a thorough characterization of this model by assessing some parameters that are not fully described in the literature, namely a precise description of skin disruption. It was evaluated by transepidermal water loss measurements and analyses of epidermis swelling as a consequence of keratinocyte hyperproliferation. The extent of neo-angiogenesis and hypervascularity in dermis were highlighted by immunostaining. Moreover, we investigated systemic inflammation through cytokines levels, spleen swelling and germinal centers appearance in draining lymph nodes. The severity of all parameters was correlated to IMQ concentration in skin samples. This study outlines new parameters of interest useful to assess this model. We highlight the skin barrier disruption and report a systemic inflammatory reaction occurring at distance both in spleen and lymph nodes. These newly identified biological endpoints could be exploited to investigate the efficacy of therapeutic candidates for psoriasis and more extensively for several other skin inflammatory diseases.

• angiogenesis
• imiquimod
• imiquimod quantification in skin
• lymph nodes
• mouse model
• psoriasis
• spleen
• transepidermal water loss

The aim of the study was to evaluate concentrations of IL-17 in the serum and plaque scales of psoriatic patients. We analyzed their association with the clinical activity of the disease and with body mass index (BMI). Demographic data, medical history, serum, and scale from psoriatic plaques for assessment of IL-17 were collected from all the participants. The disease severity was assessed with PASI (Psoriasis Area and Severity Index), BSA (Body Surface Area), PGA (Physician Global Assessment), NAPSI (Nail Psoriasis Severity Index), and DLQI (Dermatology Quality of Life Index) scores. Obesity was diagnosed by calculating body mass index. Serum and scale concentration of IL-17 was determined with Human IL-17A High Sensitivity ELISA kit and Human IL-17 ELISA kit. In the psoriatic patients, BMI was statistically significantly higher than in the control group. Most of the patients presented BMI higher than normal. Our study confirms that overweight is a problem among psoriatic patients. A significant positive correlation between the IL-17 serum and scale concentrations and psoriasis severity indicates that IL-17 can be used as the marker of disease severity. More data from human studies can be crucial for understanding that relationship between IL-17, psoriasis, and obesity.

• lipids
• psoriasis
• psoriatic arthritis
• serum interleukin 6

• Psoriasis
• biologic therapies
• cytokines
• immunity
• lymphocytes

Psoriasis is a multifactorial disease with a dysregulation in immune system. The aim of this study was to survey the clinical efficacy and safety of muramyl peptide—the ligand of the receptors of innate immunity (drug Licopid, AO Peptek, Moscow, Russia) in patients with psoriasis. The effect of muramyl peptide on 86 patients with different severity of plaque psoriasis was tested. The Psoriasis Area and Severity Index (PASI), cytokine status and production of nitric oxide in blood serum, and the subsequent course of psoriasis have been evaluated. Evaluation of significance of observed differences was presented by the Student's t-test. As a result of the treatment, clinical cure or improvement was detected in 98.2% of patients (p < 0.05), while 24.4% had a complete cure. Subsequent observations during 4 years showed that patients who received muramyl peptide statistically significantly increased relapse-free period. Moreover, subsequent relapses of the disease after treatment with muramyl peptide were in much more milder form in the cases of mild psoriasis. The conducted studies showed that monotherapy with muramyl peptide stopped the clinical manifestations of psoriasis, normalized the processes of cytokine-dependent [interleukin (IL)−4, IL-10, IL-12, tumor necrosis factor alpha (TNF-α)] regulation of the immune response and nonspecific resistance, expressed in a decreasing amount of serum antigens sCD54 [soluble intercellular adhesion molecule-1 (sICAM-1)] to reference values (p ≤ 0.01). Taken together, our research demonstrated the effectiveness of therapy with muramyl peptide and moreover, that elevated levels of sCD54 and MIF (p ≤ 0.01) in the serum of patients with psoriasis considered as potential biomarkers of the severityof psoriasis and control over their dynamics have prognostic significance in determining the effectiveness of the therapy.

• IL-10
• IL-12
• IL-4
• MIF
• TNF-α
• muramyl peptide
• psoriasis
• sCD54

• mean platelet volume
• metabolic syndrome
• platelet distribution width
• psoriasis vulgaris

Psoriasis and depression may have common mechanisms, such as systemic inflammation, dysfunction of the hypothalamic-pituitary-adrenal axis, and vitamin D₃ deficiency. Among men with psoriasis, this study examined whether depression severity was associated with serum concentrations of different metabolic and inflammatory markers.

The study included 85 men with psoriasis (mean age ± standard deviation [SD], 47 ± 14 years) and 65 men without psoriasis (mean age ± SD, 44 ± 13 years). In both groups, we measured the body mass index; blood pressure; and serum concentrations of lipids, uric acid, lipase, interleukins 6 and 18, cortisol, and 25-hydroxyvitamin D₃. All participants completed the Beck Depression Inventory. Other variables analyzed included psoriasis duration, the Psoriasis Area Severity Index, and the percentage of body surface area affected by psoriatic lesions.

Compared with controls, patients with psoriasis had significantly greater depression severity, higher body mass indices, and higher serum concentrations of total cholesterol and interleukins 6 and 18; moreover, they had significantly lower serum 25-hydroxyvitamin D₃ concentrations. In patients with psoriasis, depression severity correlated positively with psoriasis duration, the Psoriasis Area Severity Index, the percentage of body surface area affected by psoriatic lesions, and interleukin-18 concentration. In patients with psoriasis, depression severity correlated negatively with 25-hydroxyvitamin D₃ concentration, but it did not correlate significantly with the serum concentrations of interleukin 6 and cortisol.

High concentrations of interleukin 18 and low concentrations of 25-hydroxyvitamin D₃ may be associated with depression severity in men with psoriasis. Thus, further studies should examine whether effective anti-inflammatory treatments or vitamin D₃ supplementation can improve depression outcomes in these patients.

• cytochrome P450
• disease-drug interaction
• high-affinity humanized IgG1k antibody
• interleukin-23
• psoriasis
• tildrakizumab

• Adalimumab
• Psoriasis
• Squamous cell carcinoma antigen

This study aims to assess how mean corpuscular volume (MCV), red cell distribution width (RDW), and thiol-disulphide homeostasis are altered in psoriasis patients. This is a cross-sectional review of 76 healthy volunteers and 87 psoriasis patients who were consecutively admitted to the department of dermatology. Psoriasis patients and healthy controls were statistically similar with respect to age, sex, body mass index, blood pressures, and disease duration (p > 0.05 for all). When compared to healthy controls, psoriasis patients had significantly higher MCV, RDW, C-reactive protein (CRP), disulphide, disulphide/native thiol, and disulphide/total thiol (p < 0.001 for all). However, psoriasis patients had significantly lower native thiol and native thiol/total thiol (p = 0.009 and p < 0.001, respectively). When compared to healthy controls, the patients with Psoriasis Area Severity Index (PASI) ≤ 10 and patients with PASI > 10 had significantly higher MCV, disulphide, disulphide/native thiol, and disulphide/total thiol (p < 0.001 for all). The patients with PASI ≤ 10 and patients with PASI > 10 had significantly lower native thiol/native thiol than healthy controls (p < 0.001 for all). The psoriasis patients with PASI > 10 had significantly higher RDW and CRP than healthy controls and patients with PASI ≤ 10 (p < 0.001 for all). Disulphide, disulphide/native thiol, disulphide/total thiol, and native thiol/total thiol correlate significantly with both PASI scores and disease duration. Thiol-disulphide homeostasis is enhanced in psoriasis patients. Ongoing inflammation and increased oxidative stress in psoriasis patients also trigger the formation of prooxidants which are neutralized by antioxidants such as thiols. That is why plasma thiol levels are decreased in psoriasis patients.

• astilbin
• psoriasis
• interleukin-6
• interleukin-22
• p38 mitogen-activated protein kinase
• keratinocyte

• Animals
• Anti-Inflammatory Agents/pharmacology
• Cell Line, Transformed
• Disease Models, Animal
• Ear
• Emulsions
• Flavonols/pharmacology
• Gene Expression Regulation
• Guinea Pigs
• Humans
• Immunologic Factors/pharmacology
• Interleukin-17/antagonists & inhibitors
• Interleukin-17/genetics
• Interleukin-17/immunology
• Interleukin-6/antagonists & inhibitors
• Interleukin-6/genetics
• Interleukin-6/immunology
• Interleukins/antagonists & inhibitors
• Interleukins/genetics
• Interleukins/immunology
• Keratinocytes/drug effects
• Keratinocytes/immunology
• Keratinocytes/pathology
• Lipopolysaccharides/antagonists & inhibitors
• Lipopolysaccharides/pharmacology
• Male
• Mitogen-Activated Protein Kinase 1/genetics
• Mitogen-Activated Protein Kinase 1/immunology
• Mitogen-Activated Protein Kinase 3/genetics
• Mitogen-Activated Protein Kinase 3/immunology
• Phosphorylation/drug effects
• Propranolol/administration & dosage
• Psoriasis/chemically induced
• Psoriasis/drug therapy
• Psoriasis/genetics
• Psoriasis/pathology
• Signal Transduction
• p38 Mitogen-Activated Protein Kinases/genetics
• p38 Mitogen-Activated Protein Kinases/immunology
• Interleukin-22

• adipokine
• cytokine
• meta-analysis
• psoriasis
• serum

Epidemiological studies suggest an increased prevalence of cardiovascular disease (CVD) in patients with psoriasis (PS). Therefore, emphasis has lately been laid on the necessity for clinical evaluation of the risk of CVD in these patients. The systemic inflammatory markers C-reactive protein (CRP) and interleukin- (IL-) 6, which have long been used to predict future CVD in the general population, are increased manyfold in patients with PS. Lipid abnormalities characterized by elevated triglycerides, low HDL cholesterol, and higher concentrations of LDL cholesterol and its oxidized form are also prevalent in patients. There is a need for additional laboratory markers for the assessment of cardiovascular status of patients with PS. Due to frequent comorbid overweight and obesity, biologically active compounds produced by adipocytes may have an impact on monitoring the status of the cardiovascular system of patients with PS. For this purpose, two adipokines, adiponectin and leptin, have been most extensively studied. The review focuses on some inflammatory and oxidative stress aspects in patients with PS through the analysis of the impact of prominent adipokines and oxidized low-density lipoprotein (oxLDL) to assess their eligibility for clinical practice as markers of CVD risk in patients with PS.

Although phenotypic heterogeneity of psoriasis is suggested by the alternate activation of either T-helper (Th)1-related or Th17-related cytokines, little is known about the mRNA levels of inflammatory cytokines.

To investigate whether there is differential expression of Th1-related and Th17-related inflammatory cytokine genes 1) between psoriatic patients and healthy controls, and 2) between patients with different psoriasis phenotypes.

Twenty-five patients with psoriasis (10 with guttate psoriasis and 15 with plaque psoriasis) and 5 healthy volunteers were enrolled in this study. The mRNA levels of circulating cytokines (interleukin [IL]-2, IL-12p40, interferon-γ, IL-17A, IL-22, and IL-23R) were measured by real-time reverse transcription polymerase chain reaction.

The comparison between psoriatic and healthy control samples revealed that IL-12p40, IL-17A, and IL-22 mRNA levels were significantly higher (approximately 4∼6 folds) in the patients with psoriasis. The mRNA levels of these six cytokines in the blood did not differ between the guttate and plaque psoriasis groups.

We found that the mRNA levels of blood inflammatory cytokines (IL-12p40, IL-17A, and IL-22) were significantly elevated in patients with psoriasis compared to the levels in healthy controls, but they did not significantly differ between patients with guttate and plaque type psoriasis.

• Cytokines
• Gene expression
• Psoriasis

• comorbidity
• leukocyte recruitment
• neutrophil extracellular trap
• neutrophilic granulocytes
• psoriasis

Psoriatic keratinocytes express exaggerated levels of inflammatory cytokines, and show aberrant hyperproliferation and terminal differentiation in the pathogenesis of psoriasis. The antimicrobial protein hS100A7 (psoriasin) has been found highly expressed in psoriatic skin, but the mechanism and physiological function remain largely unknown. We observed that hS100A7 induces mature interleukin 1α (17kDa) expression in normal human epidermal keratinocytes, which is dependent on RAGE-p38 MAPK and calpain-1 as the inhibitors or knockdown of them completely decreased the expression of mature interleukin1α. Then, we proved mS100a7a15, mature IL-1α and calpain-1 were highly expressed in imquimod-induced psoriasis model and mouse IL-17a-neutralizing antibody treatment attenuated mS100a7a15 expression. At last, PD 151746 (calpain-1 inhibitor) treatment decreased epidermal thickness in imquimod-induced psoriasis model. Taken together, our results suggest that mature IL-1α induced by hS100A7 is via RAGE-p38 MAPK and calpain-1 pathway in keratinocyte and this mechanism may play an important role during psoriasis.

• Acrylates/pharmacology
• Animals
• Calpain/metabolism
• Cell Line
• Disease Models, Animal
• Gene Expression
• Humans
• Hyperplasia
• Interleukin-1alpha/genetics
• Interleukin-1alpha/metabolism
• Keratinocytes/metabolism
• Mice
• Proteolysis
• Psoriasis/genetics
• Psoriasis/metabolism
• Psoriasis/pathology
• Receptor for Advanced Glycation End Products/metabolism
• S100 Calcium Binding Protein A7
• S100 Proteins/metabolism
• p38 Mitogen-Activated Protein Kinases/metabolism

• Cytokines
• Dopamine
• Keratinocytes
• Macrophages
• Metalloproteinase
• NFκB
• β-Adrenergic receptors

• Adrenergic beta-Antagonists/pharmacology
• Cell Line
• Cell Movement/drug effects
• Cell Movement/physiology
• Dopamine/pharmacology
• Dose-Response Relationship, Drug
• Humans
• Keratinocytes/drug effects
• Keratinocytes/physiology
• Macrophages/drug effects
• Macrophages/physiology
• Receptors, Adrenergic, beta/physiology
• Wound Healing/drug effects
• Wound Healing/physiology

• Dendritic cells
• Psoriasis
• TLR7/8
• β,β-dimethylacryloyl alkannin

• Animals
• Cell Differentiation/drug effects
• Cells, Cultured
• Dendritic Cells/drug effects
• Dendritic Cells/immunology
• Disease Models, Animal
• Humans
• Imidazoles/pharmacology
• Interleukin-1 Receptor-Associated Kinases/metabolism
• Interleukin-1beta/genetics
• Interleukin-1beta/metabolism
• Interleukin-23/genetics
• Interleukin-23/metabolism
• Lithospermum
• Male
• Membrane Glycoproteins/agonists
• Membrane Glycoproteins/metabolism
• Mice
• Mice, Inbred BALB C
• Myeloid Differentiation Factor 88/metabolism
• Naphthoquinones/chemistry
• Naphthoquinones/therapeutic use
• Psoriasis/drug therapy
• Skin/drug effects
• Skin/immunology
• Toll-Like Receptor 7/agonists
• Toll-Like Receptor 7/metabolism
• Toll-Like Receptor 8/agonists
• Toll-Like Receptor 8/metabolism

Risk of cardiovascular disease is increased in patients with psoriasis, but molecular mechanisms linking the two conditions have not been clearly established. Lack of appropriate animal models has hampered generation of new knowledge in this area of research and we therefore sought to develop an animal model with combined atherosclerosis and psoriasis-like skin inflammation.

Topical 12-O-tetradecanoylphorbol-13-acetate (TPA) was applied to the ears twice per week for 8 weeks in atherosclerosis-prone apolipoprotein E deficient (ApoE^−/−) mice.

TPA led to localized skin inflammation with increased epidermal thickness, infiltration of inflammatory-like cells and augmented tissue interleukin-17F levels. Systemic effects of the topical application of TPA were demonstrated by increased plasma concentration of serum amyloid A and splenic immune modulation, respectively. However, atherosclerotic plaque area and composition, and mRNA levels of several inflammatory genes in the aortic wall were not significantly affected by TPA-induced skin inflammation.

TPA-induced psoriasis-like skin inflammation in atherosclerosis-prone ApoE^−/− mice evoked systemic immune-inflammatory effects, but did not affect atherogenesis. The results may question the role of psoriasis-induced inflammation in the pathogenesis of atherosclerosis in psoriasis patients.

The online version of this article (doi:10.1186/s12895-016-0046-1) contains supplementary material, which is available to authorized users.

• ApoE−/− mouse
• Atherosclerosis
• Immune cells
• Inflammation
• Interleukin-17
• Psoriasis

• Cytokines
• Peripheral blood mononuclear cells
• Phototherapy
• Psoriasis
• Systemic inflammation

• IL-17
• brodalumab
• ixekizumab
• psoriasis
• secukinumab

• SQGD
• Th1/Th2cytokine
• growth factors
• immunosuppression
• γ-irradiation

• Animals
• Bacillus/chemistry
• Benzoquinones/pharmacology
• Cytokines/blood
• Gamma Rays/adverse effects
• Glucosides/pharmacology
• Hematopoiesis/drug effects
• Male
• Mice, Inbred C57BL
• Radiation-Protective Agents/pharmacology

Psoriasis is a chronic inflammatory immune-mediated skin disease, frequently associated with systemic comorbidities. According to recent data, patients with psoriasis show a greater prevalence of metabolic syndrome, which confers a higher cardiovascular risk. The link between these pathological conditions appears to be a chronic low-grade inflammatory status. The aim of this review is to focus on the multiple epidemiological and physio-pathogenetic aspects linking non-alcoholic fatty liver disease, psoriasis, and cardiovascular disease.

• Psoriasis
• Non-alcoholic fatty liver disease
• Cardiovascular risk