Sera Of Psoriatic Patients Research Articles

The Impact of Disease Severity on the Serum Levels of Significant Neutrophil Extracellular Trap (NET) Proteins in Patients with Psoriasis.

Psoriasis is an inflammatory skin disease with various symptoms of differing severities and with the reported prominent involvement of neutrophil extracellular traps (NETs). The excitation of neutrophils, e.g., by interleukin 8 (IL-8) or lipopolysaccharide (LPS), leads to the citrullination of histones and the release of protein-DNA complexes into the extracellular space, where they are digested by DNases. Our aim was to explore data on the levels of protein-complexed DNAs neutrophil elastase-DNA (NE-DNA) and myeloperoxidase-DNA (MPO-DNA), citrullinated histones (citH2, citH3, citH4), and NET-degrading enzyme DNase I in the serum of psoriatic patients with varying severities of clinical symptoms assessed with the Psoriasis Area Severity Index (PASI), Body Surface Area (BSA), and Dermatology Life Quality Index (DLQI) scores. The levels of factors were detected in 52 patients with psoriasis and 22 healthy volunteers by the enzyme-linked immunosorbent assay (ELISA). The results showed the elevated levels of NE-DNA, MPO-DNA, citH3, and DNase I in the patients with psoriasis compared to healthy volunteers (p < 0.05). Additionally, changes were noticed in the levels of NE-DNA, citH3, and DNase I, depending on the severity of symptoms (p < 0.05). In mild psoriasis (PASI < 10, BSA < 10, DLQI < 10), the suppressing activity of the enzyme caused the impaired ability to remove the physiological level of NETs, whereas in moderate to severe psoriasis (PASI ≥ 10, BSA ≥ 10, DLQI ≥ 10), the enhanced activity of DNase I failed to remove NETs due to the observed overexpression. It may, thus, be concluded that the mechanism of action of NETs, which play an undeniable role in psoriatic diseases, seem to follow two different paths depending on the severity of disease, which may be crucial in selecting potential anti-NET treatment methods.

Crosstalk between Serum and Skin Sphingolipids in Psoriasis.

Psoriasis is a chronic, complex, immunological disorder, which may lead to many different systemic complications. Sphingolipids, including ceramide, are bioactive lipids, which take part in the regulation of immune reactions, cell growth, and apoptosis. Twenty psoriatic patients and twenty-eight control subjects were included in the study. Skin (both lesional and non-lesional) and serum samples were collected from both the control group and the psoriatic patients. The levels of sphingosine (SFO), sphingosine-1-phosphate (S1P), sphingomyelin, sphinganine (SFA), sphinganine-1-phosphate (SFA1P), and ceramide (CER) were assessed in both tissue (t) and serum (s) samples using high-performance liquid chromatography (HPLC). We identified elevated serum levels of SFO, S1P, SFA, and SFA1P in psoriatic patients when compared to healthy individuals. As far as the lesional skin and serum of psoriatic patients are concerned, we demonstrated positive associations between CER_t and CER_s, SFA_t and CER_s, and SFO_t and CER_s. Additionally, we found negative correlations in the non-lesional skin and serum of psoriatic patients, including SFO_t vs. SFO_s, CER_t vs. SFA_s, CER_t vs. SFO_s, and SFO_t vs. SFA_s. Finally, we observed a positive correlation between S1P and SFA1P in both the serum samples of psoriatic patients and the serum samples of the control group. In this study, we did not observe any correlations between psoriasis area and severity index (PASI) scores and sphingolipid levels. In conclusion, our findings indicate an interplay between skin and serum lipids in psoriatic patients, which is not observed in healthy individuals.

TL1A control of eczema and psoriasis

Abstract Psoriasis is a Th17-induced dermatitis, characterized by epidermal thickening. Psoriasis increases the risk of developing arthritis and cardiovascular-related morbidities, hence the need to stop its progression early. Why the disease is patchy, and what activates the keratinocytes in the psoriatic plaques driving a Th17-type inflammation, remain unknown. Chronic exposure to imiquimod (IMQ) drives psoriasis in mice reminiscent of human disease. We have preliminary data implicating the TNFSF (tumor necrosis factor superfamily) member TL1A (tumor necrosis factor-like cytokine 1A) in psoriasis. Our loss of function studies show that the genetic deletion of TL1A receptor, protects from IMQ-induced psoriasis. Further, TL1A is known to be enriched in the psoriatic lesions and serum of psoriatic patients. These findings suggest that TL1A may play a central role in the development and maintenance of psoriasis. Therefore, targeting TL1A could be beneficial to treat Psoriasis.

MiRNA-559 and MTDH as possible diagnostic markers of psoriasis: Role of PTEN/AKT/FOXO pathway in disease pathogenesis

Psoriasis is a persistent, inflammatory, autoimmune skin disorder which can be elicited by genetic and environmental factors. Several microRNAs (miRNAs) that are abnormally expressed in psoriasis have emerged as an interesting candidate in psoriasis pathogenesis. However, the expression profile and function of miRNA-559, and its direct target metadherin (MTDH), in psoriasis need to be further illuminated. This study intended to assess miRNA-559 and MTDH levels in skin and sera of psoriatic patients and to investigate their clinical significance in an attempt for developing novel distinct tools for early diagnosis of psoriasis. Moreover, this study aimed at exploring participation of miRNA-559 in regulating MTDH/PTEN/AKT pathway in psoriasis. Expression levels of miRNA-559, AKT, FOXO1 and PTEN were measured by real-time qRT-PCR, whereas MTDH and p27 levels were assessed by ELISA in lesional, non-lesional tissues and serum of 20 psoriatic patients and 20 matching controls. Correlation study was conducted between different parameters. The diagnostic performance of miRNA-559 and MTDH in psoriasis was estimated by receiver operating characteristic (ROC) curve analysis. Expression of miRNA-559 in psoriatic patients was significantly downregulated in both lesional tissues and serum as compared to controls. Conversely, MTDH protein level showed significant increase in both tissues and serum of psoriatic patients and was inversely correlated with miRNA-559 level. Meanwhile, levels of PTEN, AKT and FOXO1 were dramatically changed in psoriatic patients compared to controls. Furthermore, serum miRNA-559 and MTDH displayed comparable diagnostic accuracy in discriminating psoriatic patients from controls. Yet, miRNA-559 demonstrated superior diagnostic performance than MTDH in psoriasis diagnosis. Together, the current findings provide the first suggestion of a new mechanism by which downregulation of miRNA-559 might induce proliferation in psoriasis through modulating PTEN/AKT/FOXO1 pathway by positive regulation of MTDH. Thus, miRNA-559 and MTDH might be proposed as promising diagnostic biomarkers of psoriasis.

Serum immunoglobulin E and Interleukin-17 levels in patients with chronic plaque psoriasis: A case-control study.

Psoriasis is a skin disorder mainly mediated by T helper (Th)-1 and Th-17 cells. Recently, high serum immunoglobulin (Ig)-E levels were detected in psoriatic patients. The etiopathogenesis of IgE overproduction in psoriatic patients is still unknown, but IL-17 has been suggested to be responsible for this abnormality. To compare levels of IgE and IL-17 in the sera of patients with chronic plaque psoriasis (CPP) to healthy subjects. This study included 40 patients with CPP and 40 age- and sex-matched healthy individuals. Serum IgE and IL-17 concentrations were measured using the enzyme-linked immunosorbent assay (ELISA) technique. Levels of IgE and IL-17 were significantly higher in the sera of psoriatic patients than in controls (p= 0.001 and 0.024, respectively). Psoriatic patients with abnormally high serum IgE levels had higher serum IL-17 levels than those with normal serum IgE levels, but the difference was statistically insignificant (p= 0.080). Furthermore, no significant correlation was found between serum IgE and IL-17 concentrations in psoriatic patients (p= 0.385). It is possible that IgE and IL-17 interact in psoriasis pathogenesis; however, this was not evident in the current study, possibly due to the small sample size. Therefore, other potential causes of elevated IgE levels in psoriatic patients should be investigated. Moreover, the interaction between IgE and IL-17 should be investigated in patients with other clinical variants of psoriasis.

Changes in Tumor Necrosis Factor α (TNFα) and Peptidyl Arginine Deiminase 4 (PAD-4) Levels in Serum of General Treated Psoriatic Patients

Psoriasis is an autoimmune disease in which the disturbed dependencies between lymphocytes, dendritic cells, keratinocytes and neutrophils play the most important role. One of them is the overproduction of neutrophil extracellular traps (NETs). The release of NETs can be induced by pathogens, as well as antibodies and immune complexes, cytokines and chemokines, including TNFα. The first step of the NET creation is the activation of peptidyl arginine deiminase 4 (PAD-4). PAD-4 seems to be responsible for citrullination of histones and chromatin decondensation, but the data on PAD-4 in NETs is inconclusive. Thus, the current study aimed to determine PAD-4 and TNFα levels in the serum of psoriatic patients by ELISA and observe the response of these factors to systemic (anti-17a, anti-TNFα and methotrexate) therapies. Increased levels of both PAD-4 and its main stimulus factor TNFα in pre-treatment patients have been reported along with the concentrations of proteins correlated with disease severity (PASI, BSA). Before treatment, the irregularities in the case of anti-nuclear antibodies level (ANA) were also observed. All of the applied therapies led to a decrease in PAD-4 and TNF levels after 12 weeks. The most significant changes, both in protein concentrations as well as in scale scores, were noted with anti-TNFα therapy (adalimumab and infliximab). This phenomenon may be associated with the inhibition of TNF production at different stages of psoriasis development, including NET creation. The obtained data suggest the participation of PAD-4 in the activation of neutrophils to produce NETs in psoriasis, which may create opportunities for modern therapies with PAD inhibitors. However, further exploration of gene and protein expression in psoriatic skin is needed.

Comparative Analysis of Levels of Iron, Copper, Transferrin, and Ceruloplasmin in Serum of the Patients of Psoriasis

Objective: To conduct a comparative analysis on the serum levels of transferrin, ceruloplasmin, copper, and iron in the serum of patients suffering from psoriasis. Methodology: It was a case-controlled comparative study conducted on a group of 40 individuals suffering from psoriasis, and another group of 40 healthy individuals. The levels of iron, copper, ceruloplasmin, and transferrin in serum were evaluated directly. The severity of the disease was observed by psoriasis area and severity index (PASI), and the association between PASI score and disease severity. Results: The study involved 40 psoriatic patients, and 40 healthy individuals, and it was observed that iron, and transferrin levels were statistically low in the patients suffering from psoriasis as compared to healthy individuals. However, there was no significant difference observed between the two groups in terms of levels of copper in serum. Conclusion: The study concluded that there is an involvement of trace elements in the serum of psoriatic patients.

Tissue and serum lipoxin A4 levels in psoriasis patients and their relation with disease severity

Background Psoriasis disease is a chronic hyperproliferative inflammatory disease, in which genetic and environmental factors have an important role, but the exact cause is yet unknown. Lipoxin A4 plays a role in improvement of psoriasis cases, it blocks the production of the proinflammatory cytokine tumor necrosis factor with increasing the production of the anti-inflammatory cytokine, c–c chemochine receptor-5 by T lymphocytes, and it reduces the perception of pain due to inflammation. Aim Detection of the expression of lipoxin A4 in the tissue and serum of psoriatic patients as compared with normal-control persons to investigate the possible role of lipoxin A4 in the psoriasis pathogenesis and its correlation with disease severity. Patients and methods The present study included 25 psoriatic patients and 25 age, sex-matched healthy controls. Four-mm punch-skin biopsy was taken from patients (psoriatic lesion) and control persons and it was kept in lysis solution for the stability of the studied parameters and it was kept frozen at –80°C till analysis of lipoxin A4 by PCR. Peripheral blood samples for detection of serum lipoxin A4 were taken. Blood samples were centrifuged and the serum was stored at –80°C and used for enzyme-linked immunosorbent assay. Results Psoriatic patients had significantly lower tissue and serum lipoxin A4 levels as compared with normal-control persons. Conclusions Lipoxin A4 could contribute to psoriasis pathogenesis through its immunomodulatory role.

Assessment of Selected Matrix Metalloproteinases (MMPs) and Correlation with Cytokines in Psoriatic Patients.

Metalloproteinases (MMPs) and cytokines have a great impact on the pathogenesis of psoriasis. Cytokines, as key mediators of inflammation and autoimmune processes, play a crucial role in the regulation of MMP expression in different cell types. Parallel, MMPs have an influence on cytokine production. This interaction was not well recognized in psoriatic patients. Our study is aimed at assessing the selected serum MMP levels and their correlations with cytokine levels in the serum of psoriatic patients. We observed a significantly elevated level of pro-MMP-1 and MMP-9 in psoriatic patients' serum in comparison to the control group. We did not observe any statistically significant differences of MMP-3 and pro-MMP-10 between the psoriatic patients and the control group. We did not observe any statistically significant differences in all the studied MMP levels between the patients with and without psoriatic arthritis (PsA). MMP-3 level correlated positively with proinflammatory cytokines, i.e., IL-12p/70, IL-17A, and TNF-α as well as MMP-3 and pro MMP-1 correlated positively with IL-4 in the psoriatic patients. In the control group, a positive correlation between pro-MMP-1 and TNF-α was found. These results confirm MMPs and Th1 and Th17 cytokine interaction in the inflammatory regulation in psoriasis.

The role of LncRNA MALAT-1 and MiRNA-9 in Psoriasis

BackgroundPsoriasis is a chronic skin disorder manifested by recurrent episodes of scaly, red, itchy skin patches that occur within apparently normal skin. ObjectivesThis study was performed to detect the expression of serum and tissue (lesion and non-lesion) LncRNA MALAT-1 and MiRNA-9 that might be used as biomarkers for psoriasis. MethodsBlood samples were obtained from 60 psoriasis patients and 40 controls, as well as 4 mm punch biopsy from lesional and non lesional skin of psoriatic patient and normal skin of healthy controls. Expression of LncRNA MALAT-1 and miRNNA-9 in serum and tissues was detected by real time qRT-PCR. Resultsa statistically significant increase in the expression of MALAT-1 in lesional and non-lesional skin and serum of psoriatic patients in comparison to controls were detected. Moreover, there was statistically significant increase in serum MiRNA-9 in patients in comparison to controls, while its tissue level was significantly lower in patients. ConclusionThis study highlights the dysregulation of LncRNA MALAT-1 and miRNA-9 in psoriasis. Elevated expression of MALAT-1 in lesional skin of psoriatic patients compared to non-lesional skin may possibly contribute to the development of psoriatic plaques.

Evaluation of Serum Level of Netrin 1 in Psoriatic Arthritis

Psoriasis is resistant interceded persistent and repetitive, fiery dermatosis skin infection. netrin 1 has a significant part in the pathogenesis of a few immune system sicknesses. This examination is intended to assess the conceivable job of Netrin 1 in the pathogenesis of psoriasis by estimating its level in the serum of psoriatic patients and associate its level with the seriousness. which may help later on treatment of psoriatic injury. This examination included 60 patients experiencing psoriasis vulgaris . Furthermore, 30 obviously solid people of coordinated with age and sex will be picked as a benchmark group. All patients will be exposed to finish history, complete general and dermatological clinical assessment will be finished. Assessment of serum level of netrins 1 in patients and control bunches by ELISA. By contrasting the two gatherings of patients and controls in this investigation there was a huge reduction in the mean serum level of Netrin1 in psoriatic patients contrasted and controls. There was high critical positive connection between's PASI score (seriousness of disease)and level of infection ,while there was no huge relationship between's PASI score and illness span or age. There was high huge negative connection between's Netrin1 level and degree likewise there was critical negative relationship between's Netrin1and Disease span while there was no huge relationship between's Netrin 1 and age and sex. There is a part of Nerrin1 in the pathogenesis of psoriasis.Netrin1 can be utilized as marker of sickness degree and illness length.

Neurotransmitter imbalance in serum of psoriatic patients in exacerbation stage with comorbid psychoemotional disorders.

The role of psychological factors in the manifestation and exacerbation of psoriasis is well known. Acute and chronic stress, anxiety, and depression affect the reactions of innate and acquired immunity. The exacerbations of psoriatic lesions are accompanied by increased production of inflammatory mediators, which could contribute to the imbalance of neurotransmitters and the development of symptoms of depression and anxiety. The role of inhibitory neurotransmitters in the serum of patients with psoriasis exacerbation with comorbid emotional disorders is assessed. Forty patients with psoriasis in the exacerbation stage were examined. Spielberger State-Trait Anxiety Inventory (STAI) and the Beck Depression Inventory (BDI) scale were used to assess anxiety and depression parameters. We also evaluated the concentration of serotonin and gamma-aminobutyric acid (GABA) in the serum. Patients with psoriasis had significant anxiety and depressive disorders. An imbalance in serotonin levels and a decrease in serum GABA levels in patients with psoriasis in the acute stage were noted. Only patients with anxiety disorder had increased serotonin levels. Our findings suggest that the imbalance of neurotransmitters in patients with psoriasis in the acute stage is important in predicting the development of the emotional well-being.

026 The impaired suppressive activity and altered response to IL-33 of regulatory T cells in a psoriasis model may be due to decreased ST2 expression

Interleukin 33 (IL-33), initially described as an alarmin, is released by cells following cell damage. It fulfills numerous functions in infections and inflammatory diseases by modulating both the innate and the adaptive immune system. IL-33, however, can also act in an immunosuppressive fashion by inducing regulatory T cells (Treg). Enhanced IL-33 levels are found both in the skin and the serum of psoriatic patients. On the other hand, in psoriasis Treg appear to be impaired in their suppressive function. To study whether “psoriatic” Treg are impaired in their response to IL-33, we utilized the imiquimod (IMQ)-induced psoriasis like model. IL-33 expression was elevated in both skin and serum of IMQ-treated mice, as demonstrated by in situ immunofluorescence staining and ELISA. However, the suppressive activity of Treg obtained from IMQ-mice was reduced as indicated by adoptive transfer experiments. To study whether the response of Treg to IL-33 is altered in IMQ-mice, Treg from untreated or IMQ-mice were incubated with IL-33 and injected into naïve mice which were sensitized thereafter. The suppressive capacity of Treg obtained from untreated mice could be further enhanced by IL-33, whereas Treg from IMQ-mice did not respond to IL-33. IL-33 exerts its activity via binding to its receptor ST2. ST2 expression identifies a highly activated, strongly suppressive Treg subset, which is superior to ST2− Treg in suppressing CD4+ T cell proliferation. FACS analysis of Foxp3 +CD4+CD25+ cells revealed that ST2 expression on IMQ-Treg was down-regulated in comparison to Treg from untreated animals. Decreased expression of the IL-33 receptor could be an explanation for the weaker response of Treg to IL-33 in IMQ-treated mice and their reduced suppressive activity. Further studies have to elucidate the mechanism by which ST2 expression is down-regulated in the IMQ-model and whether reduced ST2 expression can be also observed in psoriasis.

014 Psoriatic regulatory T cells are impaired in their suppressive activity and respond differently to IL-33

Interleukin 33 (IL-33), initially described as an alarmin released by cells following cell damage, can also act immunosuppressive by inducing regulatory T cells (Treg). Disruption of the skin barrier by tape stripping in mice released IL-33 which induced Treg. Accordingly, contact hypersensitivity (CHS) was suppressed upon barrier disruption. Furthermore, blockade of IL-33 enhanced CHS, whereas injection of IL-33 suppressed CHS via induction of Treg. IL-33 is enhanced in the skin and serum of psoriatic patients. On the other hand, in psoriasis Treg are impaired in their suppressive activity. Thus, we asked whether “psoriatic” Treg are impaired in their response to IL-33 in the imiquimod (IMQ)-induced psoriasis like model. IL-33 was enhanced in skin and serum of IMQ-mice. To study the influence of IL-33 on Treg in IMQ-mice, CD4+CD25+ Treg isolated from IMQ or untreated mice were injected into naïve mice which were sensitized 24 h later. Ear challenge was reduced in mice receiving Treg from untreated donors, whereas injection of Treg from IMQ-mice did not cause suppression, implying impairment of Treg in IMQ-mice. To study the response of Treg to IL-33 in IMQ-mice, Treg from untreated or IMQ-mice were incubated with IL-33 and injected into naïve mice which were sensitized thereafter. The suppressive capacity of Treg from WT mice was further enhanced by IL-33, whereas Treg from IMQ mice did not to respond to IL-33. Treg isolated from blood of psoriatic patients were inhibited in their suppressive activity, when compared to Treg from healthy controls. IL-33 induced the expression of Foxp3 in CD4+ T cells obtained from controls, but not in T cells from psoriatic patients. These data confirm that in psoriasis Treg are functionally impaired which may be associated with an altered response to IL-33. The mechanisms responsible for this altered behavior of Treg in psoriasis remain to be elucidated.

Evaluation of Serum Adenosine Deaminase and Inflammatory Markers in Psoriatic Patients.

Background:Adenosine deaminase (ADA) is an enzyme involved in purine metabolism and it is a marker of nonspecific T-cell activation. Few studies have shown high levels of ADA in the epidermis and sera of psoriatic patients. Other inflammatory markers such as high-sensitive C-reactive protein (hsCRP), erythrocyte sedimentation rate (ESR), and serum uric acid (SUA) have shown correlations with psoriasis area severity index (PASI) score. The correlation between ADA and PASI score is still a matter of debate.Aims:The aim of this study was to evaluate serum ADA, hsCRP, SUA, and ESR in psoriatic patients and their correlation with PASI score.Patients and Methods:This study included 60 psoriatic patients divided according to PASI score into three groups (mild, moderate, and severe) each containing 20 patients. PASI score <10 was defined as mild, (10–20) moderate, and >20 severe. Twenty healthy subjects of matched age and sex were included as control. Serum ADA, hsCRP, SUA, and ESR were evaluated for patients and controls. Correlations of ADA, hsCRP, SUA, and ESR with PASI scores were done.Results:While ADA, hsCRP, SUA, and ESR showed a significant increase in psoriatic patients compared with that of the controls (P<001), they showed no significant difference between different psoriatic groups (P>0.05) and no correlations with PASI score (P>0.05). The frequency of joint affection increased with increasing severity of psoriasis (5%, 10%, and 25% in mild, moderate, and severe psoriasis, respectively).Conclusion:Serum ADA, hsCRP, SUA, and ESR showed higher levels among psoriatic patients than in controls. The increased ADA in psoriatic patients supports the role of T-cell activation and proliferative disorder in the pathogenesis of psoriasis. No significant correlations were found between these biomarkers and PASI score. Further studies are needed to validate these biomarkers as diagnostic and prognostic factors in psoriasis.

Mitochondrial dysfunction in affected skin and increased mitochondrial DNA in serum from patients with psoriasis.

Psoriasis is characterized by keratinocyte proliferation and chronic inflammation, but the pathogenesis is still unclear. Dysregulated mitochondria (mt) could lead to reduced apoptosis and extracellular secretion of mtDNA, acting as "innate pathogen" triggering inflammation. Serum was obtained from healthy volunteers and psoriatic patients. Mitochondrial DNA was extracted from the serum and amplified with quantitative PCR (qPCR). Punch biopsies were obtained from lesional and non-lesional psoriatic skin (10cm apart) and from healthy volunteers, were placed in RNA later and were stored at -80°C until RNA was extracted and cDNA was synthesized; gene expression of uncoupling protein 2 (UCP2), Dynamin-related protein 1 (Drp1) and calcineurin, involved in the regulation of mitochondria function, was detected with qPCR. Mitochondrial DNA was significantly increased (7s, P=0.0496 and Cytochrome B, CytB, P=0.0403) in the serum of psoriatic patients (n=63) as compared to controls (n=27). Gene expression was significantly reduced for UCP2 (P=0.0218), Drp1 (P=0.0001) and calcineurin (P=0.0001) in lesional psoriatic skin, as compared to non-lesional or control skin. Increased serum extracellular mtDNA in psoriatic patients and decreased expression of mitochondrial regulatory proteins in psoriatic skin suggest increased inflammation and reduced keratinocyte apoptosis, respectively. Inhibitors of mtDNA secretion and/or UCP2 stimulants may be potential treatment options.

PATHOGENIC ROLE OF CYTOKINES IN PSORIASIS

Aim. The aim of this study is determination of the role of certain pro-inflammatory and anti-inflammatory cytokines in the pathogenesis of psoriasis. Material and methods. The 110 patients with plaque form of psoriasis of moderate severity were examined, who were divided into 2 groups. Group 1 includes 65 patients (43 men and 22 women) from 18 to 64 years old with a duration of disease from 1 year to 39 years. The traditional treatment (detoxification, antioxidant, antihistamine, multivitamin, membrane stabilizing, local anti-inflammatory) was prescribed to the patients of group 1. Group 2 includes 45 patients from 18 to 65 years old (31 men and 14 women) with a duration of disease from 6 months to 32 years. The alternative treatment (with traditional therapy, the hepatoprotectors was also used) was prescribed to the patients of group 2. The control group makes 18 practically healthy periodic donors (9 men and 9 women) from 19 to 57 years old. The level of IFNγ, TNFα, IL-1α, IL-2, IL-10 and TGFβ was investigated in the serum of psoriatic patients by ELISA (commercial kits of Demeditec Diagnostics GmbH were used). Results. Before the treatment, the significant increase of level of circulating pro-inflammatory cytokines and significant decrease of level of anti-inflammatory cytokines were seen in both groups of patients with psoriasis compared with the control group. After the treatment, the level of proinflammatory cytokines is significantly reduced and the level of anti-inflammatory cytokines is significantly increased in group 1, approaching to the normal values. In group 2, the level of proinflammatory cytokines decreases more than in group 1 after the treatment. The level of anti-inflammatory cytokines also increases more than in group 1 (high treatment efficiency). The intensity of the rate of decrease of PASI after treatment in patients of group 2 is at least 1.2 times higher than in I group, of DLQI after treatment in patients of group 2 is at least 1.44 times higher than in group 1. Conclusions. The registered changes in the serum of patients with moderate severity of papular-plaque form of psoriasis indicate their essential role in the pathogenesis of psoriasis.

High mobility group box 1 is increased in the sera of psoriatic patients with disease progression.

Psoriasis vulgaris (PV) is an autoimmune-related chronic inflammatory disease, which appears mostly in skin, but also affects the vascular and metabolic system. The incidence of PV is 2-3% in the general population and there is still no possibility to cure. Trigger factors have been identified to initiate and maintain inflammation in the skin, which is characterized by Th1-, Th17- and Th22- cells. We hypothesize that the damage-associated molecular pattern (DAMP) molecule high mobility group box 1 (HMGB1) plays a role in the pathogenesis of PV. HMGB1 is a DNA-binding protein located in the nucleus, which acquires cytokine-like properties once released from the cell upon necrotic cell death or actively secreted by immune cells in inflammation and cancer. We recruited 90 psoriatic patients under and without therapy with mild, intermediate and severe progression of disease, defined by the Psoriasis Area Severity Index. Serum levels of HMGB1 in patients with PV were detected by enzyme-linked immunosorbent assay (ELISA). Our results show an increased level of HMGB1 in the sera of patients with PV in comparison to healthy donors. Furthermore, our analyses reveal that HMGB1 levels are significantly increased with disease progression and are downregulated after standard therapies for PV have been conducted. Our data provide insights into a possible role of HMGB1 for inflammation in PV.

Assessment of serum interferon-γ in psoriasis

Background Psoriasis is a common chronic, recurrent, and immune-mediated disease of the skin and joints that follows a relapsing and remitting course. Psoriasis represents a T-cell-mediated inflammatory skin disease that includes the activation of both Th1, which produces interferon-g (IFN-γ), tumor necrosis factor-α, and interleukin-2 (IL-2), and Th17, which produces IL-17, tumor necrosis factor-α, IL-6, and IL-22. Objective We planned this study to determine probable associations between IFN-γ, Th1 cytokine, in the sera of psoriatic patients and the possible correlation to disease severity. Materials and methods We studied the level of serum IFN-γ in 40 cases of plaque psoriasis, erythrodermic, and guttatepsoriasis using PASI score for assessing the severity, and in the serum of healthy 40 controls. Results There was a statistically significant positive correlation between the PASI score and the level of IFN-γ in all clinical types. This can suggest that serum IFN-g is a psoriasis severity and prognostic marker. Conclusion Serum IFN-γ in psoriatic patients can be used as a severity and prognostic marker, and then anti-IFN-γ may eventually become a useful therapeutic approach in psoriasis.

The rise of staphylococcal super antigens in psoriatic patients: a case-control study.

Background:Staphylococcus aureus, the major virulence factor of hospital and community acquired infections, secretes numerous exotoxins (super antigens), which may affect immunological and inflammatory status in psoriatic skin lesion.Objectives:This study is designed to compare the S. aureus super antigens level in sera of psoriatic patients with normal cases (nevus).Patients and Methods:A case control study was performed in dermatology ward of Rasoul Hospital in Tehran, IR Iran (2008 - 2010). Staphylococcal super antigens (Entrotoxin A, B, D and TSST1) were measured in serum of 41 psoriatic patients and 28 normal persons (Nevus) by ELISA. Chi square values (CI 95%, P value < 0.05) were calculated for all categorical variables.Results:In this study 63.4% (26) of cases were male, 36.6% (15) were female. Age ranged from 4 months to 64 years old, with a mean age of 33.7 ± 15.4 years. Type of skin disease in cases: 20% (8) were inflicted by the Gutate form of the disease; 59% (23) with chronic plaque psoriasis (CPP), 7.7% (3) with erythrodermic and 12.8% (5) had other types of the disease (plaque, pustular, inverse). TSST (toxic shock syndrome toxin) was detected in 47% (20/41) of cases and in 6% (1/28) of the controls with a significant difference. (P value = 0.000) Entrotoxins (A, B, D) were detected in the sera of 48.8% (21/41) of cases; and only 6 %( 1/21) of controls, showed significant differences (P value = 0.000) positive TSST was more common in spring, and correlates with CPP type of psoriasis, but not related to patient`s gender and age.Conclusions:In this study, S. aureus were 25 times more in psoriatic patients. Super antigens should be first detected in the serum samples; if negative, the skin lesions should be examined by PCR especially in chronic types of disease. Adding the antibiotics against S. aureus to other conventional treatments might be helpful. It has a more important and significant role in children with acuteinfection.