Skin Lesions Of Psoriasis Vulgaris Research Articles

Integrative medicine (East Asian herbal medicine combined with conventional medicine) for psoriasis: A protocol for systematic review and meta-analysis.

Psoriasis is a chronic, inflammatory, autoimmune skin disease. The aim of this review is to systematically evaluate the efficacy and safety of integrative medicine (East Asian herbal medicine combined with conventional medicine) used to treat inflammatory skin lesions of psoriasis. A comprehensive literature search will be conducted in 3 English databases (PubMed, Cochrane Library, and Embase), 4 Korean databases (Korean Studies Information Service System, Research Information Service System, Oriental Medicine Advanced Searching Integrated System, and Korea Citation Index), 2 Chinese databases (Chinese National Knowledge Infrastructure Database and Wanfang data), and 1 Japanese database (Citation Information by National Institute of Informatics) for randomized controlled trials from their inception until July 29, 2021. Statistical analysis will be performed using R version 4.1.2 and the R studio program using the default settings of the "meta" and "metafor" packages. The primary outcome will be an improvement in the psoriasis area severity index. All outcomes will be analyzed using a random-effects model to produce more statistically conservative results. If heterogeneity is detected in the study, the cause will be identified through sensitivity, meta-regression, and subgroup analyses. Methodological quality will be assessed independently using the revised tool for the risk of bias in randomized trials, version 2.0. The overall quality of evidence will be evaluated according to the Grading of Recommendations Assessment, Development, and Evaluation pro framework. This study will review all available trials on the same subject and arrive at a more statistically robust conclusion based on a sufficient sample size of participants and additional analysis using data mining techniques will be performed on intervention prescription information in clinical studies collected according to rigorous criteria. We believe that this study will provide useful knowledge on managing inflammatory skin lesions of psoriasis vulgaris using integrative medicine using East Asian herbal medicine.

Investigation of the role of IL18, IL-1β and NLRP3 inflammasome in reducing expression of FLG-2 protein in Psoriasis vulgaris skin lesions

ABSTRACT We investigated the effects of the NACHT leucine-rich repeat- and PYD-containing proteins (NLRP3) inflammasome, interleukin −18 (IL-18) and interleukin-1 beta (IL-1β) cytokines on the expression of filaggrin-2 (FLG-2) protein in psoriasis patients. Peripheral blood mononuclear cells (PBMC), including T cells, were isolated from psoriasis patients and healthy donors. Ribonucleic acid (RNA) extraction and reverse transcription-polymerase chain reaction (RT-PCR) were performed for all specimens. Immunohistochemical analysis for FLG-2 in normal and psoriatic epidermal tissue also was performed. Western blot was used to separate and identify FLG-2 protein, and immunohistochemical staining was performed to assess FLG-2 expression for psoriasis skin lesions and normal skin. RT-PCR analysis indicated that NLRP3 inflammasome, IL-18 cytokine and IL‐1β cytokine expression were increased in psoriatic epidermis compared to normal skin. We found that the expression of FLG-2 was decreased in psoriatic epidermis compared to normal skin. Higher levels of NLRP3 help decrease the FLG-2 level.

Natural killer T cells in the pathogenesis of psoriasis

Natural killer T (NKT) cells are a unique lymphocyte subpopulation that share properties and express surface markers of both NK cells and T cells. NKT cells can recognize antigens presented by CD1d molecules, secrete numerous cytokines rapidly, regulate T cell differentiation, and play an important regulatory role in autoimmune diseases. Recent pathological studies have shown obvious infiltration of lymphocytes and monocytes in skin lesions of psoriasis vulgaris. Moreover, the infiltration of T lymphocytes and dendric cells in the epidermis or dermis is an important pathological feature of psoriasis, suggesting that the immune system participates in the occurrence and development of psoriasis. At present, it is considered that psoriasis is a polygenic inflammatory dermatosis caused by the interaction of multiple factors such as genetic and environmental factors, with the pathogenesis being related to immune mediation. Key words: Psoriasis; Natural killer T-cells; Cytokines; Pathology; Immunity

Expression of cannabinoid receptor type 2 in skin lesions of psoriasis vulgaris

Objective To investigate the expression of cannabinoid receptor type 2 (CNR2) in skin lesions of psoriasis vulgaris, and to explore its significance. Methods Tissue samples were obtained from lesions and perilesional skin of 20 patients with psoriasis vulgaris, and normal skin of 10 human controls without psoriasis or other autoimmune dermatoses. Real-time fluorescence-based quantitative PCR and immunohistochemistry were performed to determine the mRNA and protein expression levels of CNR2 in these samples. Statistical analysis was carried out by using two-sample t test and chi-square test. Results CNR2 mRNA and protein were expressed in the normal control skin, lesional skin and perilesional skin tissues. As immunohistochemistry showed, CNR2 was distributed diffusedly in the prickle cell layer in lesional skin, but expressed in the basal cell layer of the epidermis in normal control skin and perilesional skin. The mRNA expression level (2-△△Ct) of CNR2 was significantly higher in lesional skin than in normal control skin and perilesional skin tissues (3.97 vs. 1.00 and 1.49, both P 0.05). The expression rate of CNR2 protein was significantly higher in lesional skin (90%(18/20) than in perilesional skin (15% (3/20), χ2=22.56, P< 0.01) and normal control skin tissues (10% (2/20), χ2=18.37, P < 0.01), while there was no significant difference between normal control skin and perilesional skin tissues (χ2=0.14, P=0.70). Conclusions The mRNA and protein expressions of CNR2 are both increased in skin lesions of psoriasis vulgaris, suggesting that CNR2 may be related to the occurrence and development of psoriasis vulgaris. Key words: Psoriasis; Genes; Receptors, cannabinoid, 2

IL-36 cytokine expression and its relationship with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions

This study examined the correlation of the expression of interleukin-36 (IL-36), a novel member of interleukin-1 (IL-1) family, with p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways in psoriasis vulgaris skin lesions. The expression levels of IL-36α, IL-36β, IL-36Γ, phosphorylated p38 MAPK, and NF-κBp65 were detected in the skin tissues of 38 psoriasis patients and 17 healthy control subjects by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. The cytokine expression levels were compared between the psoriasis group and the control group. A correlation analysis between cytokine proteins was performed in the psoriasis group. Results showed that the expression levels of IL-36a, IL-36β, IL-36Γ, phosphorylated p38 MAPK and NF-κBp65 in the psoriasis group were significantly higher than those in the control group (P<0.001). In the psoriasis group, the IL-36 cytokine expression was positively correlated with phosphorylated p38 MAPK and NF-κBp65 expression (P<0.05). A significant positive correlation was also found between the phosphorylated p38 MAPK and NF-κBp65 expression (P<0.01). It was concluded that the increased IL-36 expression is correlated with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions. All the three factors may be jointly involved in the pathogenesis and local inflammatory response of psoriasis.

Cytokine modulation of retinoic acid-inducible gene-I (RIG-I) expression in human epidermal keratinocytes

Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH/D box family proteins and designated as a putative RNA helicase, which plays various roles in gene expression and cellular functions in response to a variety of RNA viruses. The present study was designed to investigate the effects of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha on RIG-I expression in human keratinocytes, and the expression of RIG-I in skin lesions of psoriasis vulgaris, in which IFN-gamma and TNF-alpha are considered to be involved in its pathogenesis. The mRNA and protein expression of RIG-I was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Immunohistochemical staining of RIG-I was examined on psoriatic skin section. The levels of RIG-I mRNA and protein were upregulated in HaCaT keratinocytes in the presence of IFN-gamma or TNF-alpha. Immunohistochemically, RIG-I was detected in the cytoplasm of the spinous and basal layers of psoriatic skin. Our results suggest that RIG-I might operate not only as a RNA helicase but also as a mediator of the cytokine network in the inflammatory skin diseases, such as psoriasis vulgaris.

Dominant Lesional T Cell Receptor Rearrangements Persist in Relapsing Psoriasis but are Absent from Nonlesional Skin: Evidence for a Stable Antigen-Specific Pathogenic T Cell Response in Psoriasis Vulgaris

In a previous study we reported that clonally expanded T cell receptor beta-chain rearrangements characterized the T cell receptor usage in skin lesions of psoriasis vulgaris and indicated antigen-specific T cell selection. To assess the relevance of clonal T cell expansion for disease progression, we now determined if select clonal T cell receptor rearrangements persisted over time and were present in nonlesional skin. Sequential biopsies were taken from psoriatic skin lesions of two patients. V-D-J junctional regions of T cell receptor beta-chain variable region gene families 2, 3, 6, 13S1, and BV17 were cloned and sequenced, as these particular BV gene families are preferentially selected in psoriatic skin lesions. The lesional T cell receptor rearrangements were compared with the T cell receptor usage in nonlesional skin and in blood. Several T cell receptor beta-chain rearrangements with high transcript frequency in the first lesional biopsy were again found in sequential lesional biopsies taken as much as 3 y later from psoriasis relapses. Only T cell receptor beta-chain rearrangements with low transcript abundance showed variability in that several clones appeared for the first time or disappeared. Although nonlesional skin also exhibited a restricted T cell receptor usage with clonal T cell receptor rearrangements, the T cell receptor usage in lesional and nonlesional skin differed nearly completely. The select lesional recurrence of identical T cell receptor rearrangements reveals that inflammation in psoriasis involves the same clonally expanded T cell populations and the same antigens over prolonged periods of time. It hereby suggests that specifically recruited and locally expanded T cell clones are permanently involved in psoriatic inflammation and may play a crucial part in disease perpetuation.

Distribution of T-cell subsets as defined by monoclonal antibodies in skin lesions of psoriasis vulgaris.

Cryostat tissue sections from skin lesions of 16 patients suffering from chronic stationary psoriasis vulgaris were assayed for the presence of distinct T-cell subpopulations with monoclonal antibodies. Using two pan-T surface markers (M-T 4-11 and Lyt 3) the total number of infiltrating T-cells was measured. This cell population was further dissected into Leu 3a (helper/inducer) and M-T 8-11 (cytotoxic/suppressor) positive subsets. Percentages of T-cell subpopulations were within the ranges found in healthy peripheral blood and were thus regarded as normal.

Immunocompetent cells in psoriasis. In situ immunophenotyping by monoclonal antibodies.

Immunocompetent cells in exacerbating untreated psoriasis vulgaris skin lesions were immunophenotypically studied by the application of a selection of monoclonal antibodies in a two-stage immunoperoxidase technique. Epidermal changes include: focal accumulation of immunoglobulins in the stratum corneum, as demonstrated by a mixture of monoclonal anti-kappa and anti-lambda antibodies; focal accumulation of OKM-1 positive but Mo-2 negative cells high in the epidermis, reflecting granulocytes in Munro's abscesses; a marked decrease in epidermal Langerhans cells with focal abnormal clumping and smaller dendrites, as demonstrated by monoclonal anti-HLA-DR and anti-T6 (OKT-6) antibodies; and, sporadic exocytosis of mainly T1 (Leu-1), T8 (Leu-2a) positive suppressor/cytotoxic T lymphocytes. The dermal infiltrates were found to consist mainly of partically activated T1 (Leu-1), T4 (Leu-3a) positive T-helper/inducer cells with a smaller compartment of T1 (Leu-1), T8 (Leu-2a) positive suppressor/cytotoxic lymphocytes. These cells were found in close apposition to T6 (OKT-6), HLA-DR positive Langerhans cells and further accompanied by a minor compartment of OKM-1, Mo-2 positive monocytes. No B-cells or plasma cells could be demonstrated in the dermis. Natural killer cells were observed only incidentally. These results fit best with the hypothesis that psoriasis is a chronic inflammatory condition as a result of persistent stimulation of T cells by immunogen(s) of epidermal origin.