Browsing by Subject "Psoriasis"

Now showing 1 - 4 of 4
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    A Pilot of Brief Mindfulness-Based Intervention to manage emotions in patients with psoriasis
    (Universidad de Murcia. Servicio de Publicaciones, 2023) Ramos, Natalia; Jiménez, Óliver; Habicheyn Hiar, Silvia; Rivas Ruiz, Francisco; Resurrección, Davinia M.; de Troya, Magdalena
    Psoriasis is a high incidence dermatosis related to stress, and its sufferers provide an appropriate target group to carry out interventions such as those based on mindfulness, aimed at helping emotion regulation. To assess the Compassionate Emotional Accompaniment Technique (CEAT) effects within a brief mindfulness-based intervention on emotion-al coping in patients with severe psoriasisto determine the efficacy of emotional coping after the induction of a negative emotional state. Forty-four adults(59.1% were women)aged 22 -71 years (M= 51.95, SD = 11.87) with severe psoriasis were assigned randomly to the CEAT group or the Emotional Disclosurecontrol group. Subjective discomfort, cognitive ability, affect, and heart rate were assessed before and after the interven-tions, with two follow-ups at 48 hours and seven days. The results show significant statistical differences in favour of the CEAT intervention versus the Emotional Disclosure group, being more effective in the emotional management after induction and follow-up. These results encourage inter-ventions in a clinical setting with patients with severe psoriasis, so future research should consider using this intervention type to improve emotional management with this population group.
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    Estudio de genes KIR y HLA-C y de polimorfismos de citoquinas en pacientes con psoriasis
    (2015-07-03) Pardo Sánchez, José; Álvarez López, María Rocío; López Hernández, Ruth; Departamento de Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica
    La psoriasis es una enfermedad de curso crónico caracterizada por la presencia de lesiones cutáneas eritemato-escamosas, y constituye uno de los procesos dermatológicos más frecuentes. Su curso clínico es dinámico e impredecible, y en algunos casos el impacto emocional y físico en el paciente que la sufre puede ser muy importante. Su inmunopatología se basa en mecanismos complejos, donde intervienen tanto una respuesta inmunitaria adaptativa, mediada fundamentalmente por células TH17, como innata, con la participación de elementos como el TNF-α o los receptores KIR (del inglés, Killer Immunoglobulin-like Receptors). Estos receptores son expresados fundamentalmente por las células NK, y su función principal es la de inhibir la actividad citotóxica de estas células tras su unión con ligandos como HLA-C. Igualmente, se sabe que el alelo HLA-C*06 es el principal determinante genético en la psoriasis, aunque los estudios en relación con el mismo realizados en nuestro país son escasos. Existe un número creciente de observaciones que demuestran que determinados genotipos receptor-ligando KIR/HLA-C modulan la acción de las células del sistema inmunitario innato a favor de interacciones activadoras que predispondrían a enfermedades autoinmunitarias como la psoriasis. Así, con el fin de realizar una descripción inmunológica de nuestros pacientes y de valorar la participación del sistema inmunitario innato en la enfermedad, en este trabajo se realizó el tipaje de los alelos HLA-C y de los genes KIR mediante técnicas de reacción en cadena de la polimerasa (PCR), tanto en pacientes con psoriasis como en controles sanos. Además, mediante tipajes de alta resolución se determinaron los polimorfismos tipo SNP de genes que codifican citoquinas proinflamatorias involucradas en la formación de la placa psoriásica (TNF-, IL-6, INF- e IL-23). Los resultados obtenidos en este trabajo confirmaron que el alelo HLA-C*06 constituía un factor de riesgo, especialmente para la psoriasis de debut precoz o tipo I, mientras que el alelo HLA-C*07 era sugestivo de protección. Con respecto a los genes KIR, los individuos que carecían de KIR2DL1, los KIR2DL2/L2 homocigotos y los portadores de KIR2DL5 mostraban una mayor predisposición a padecer psoriasis. El gen KIR2DL5 parecía actuar de manera sinérgica con HLA-C*06 sobre la susceptibilidad a padecer la enfermedad. Además, la presencia de KIR2DS2 y KIR2DS3 en el genoma del paciente constituía un factor de riesgo más específico para la artropatía psoriásica. El estudio de la combinación de los pares receptor-ligando KIR/HLA-C reveló que la presencia simultánea del alotipo HLA-C1 no modificaba el efecto de susceptibilidad a la psoriasis observado en los individuos KIR2DL2/L2 homocigotos. Sin embargo, en los pacientes KIR2DL2/L3 heterocigotos la presencia del ligando C1 ejercía un efecto protector frente a esta enfermedad, que era además dependiente de la dosis de este ligando e independiente de la presencia del alelo HLA-C*06. Además, la combinación de KIR2DS1/ligando C2 se asociaba específicamente a la psoriasis tipo I. El estudio de los polimorfismos de citoquinas mostró que los SNPs TNF -238G>A, IL6 -174G>C e INFG +874T>A determinaban una mayor susceptibilidad a la psoriasis, especialmente la tipo I. Sin embargo, en el caso del gen TNF el efecto del alelo A podía ser subsidiario de un desequilibrio de unión con HLA-C*06. Llamaba la atención que la asociación de este alelo con la psoriasis se observaba en varones pero no en mujeres. Además, el polimorfismo IL12B -1188A>C se asociaba con un efecto protector modesto. En definitiva, los hallazgos encontrados contribuyen a confirmar el papel del par KIR/HLA-C y de algunas citoquinas como el TNF-α en la patogenia de la psoriasis, y hablan a favor de la importancia de la inmunidad innata en esta enfermedad. Abstract Psoriasis is a chronic disease characterized by the presence of erythematous and scaling skin lesions, and it is one of the most frequent dermatologic process. Its clinical course is dynamic and unpredictable, and in some cases the emotional and physical impact in patients can be very important. Its immunopathology is based on complex mechanisms, where either an adaptive immune response, mediated fundamentally by TH17 cells, and an innate immune response, with the participation of elements such TNF-α or Killer Immunoglobulin-like Receptors (KIR), are involved. These receptors are mainly expressed by NK cells, and their principal task is to inhibit these cells cytotoxic activity after their binding to ligands such as HLA-C molecules. Equally, it is known that HLA-C*06 allele is the main genetic factor in psoriasis, however studies related to this allele are hardly to be found in our country. There is a growing number of studies which demonstrate that certain KIR/HLA-C receptor-ligand genotypes modulate the action of cells from the innate immune system supporting activating interactions which would predispose to autoimmune diseases such as psoriasis. Thus, with the aim of performing an immunologic description of our patients and evaluating the participation of the innate immune system in the disease, in this study was carried out the genotyping of HLA-C alleles and KIR genes by means of polymerase chain reaction techniques, both in patients with psoriasis and in healthy controls. Besides, genotype of SNP polymorphisms of genes which codify pro-inflammatory cytokines involved in the formation of psoriatic plaques (TNF-α, IL-6, INF-γ and IL-23) were identified by high resolution techniques. The results of this study confirmed that HLA-C*06 allele is a risk factor, specially for patients with early onset psoriasis, type I, while HLA-C*07 allele suggested protection against the disease. Regarding KIR genes, individuals who lacked KIR2DL1, KIR2DL2 homozygotes and KIR2DL5 carriers, showed a higher predisposition to suffer from psoriasis. KIR2DL5 gene appeared to act synergistically with HLA-C*06 on the susceptibility to suffer from this disease. In addition, presence of KIR2DS2 and KIR2DS3 in patient’s genome constituted a more specific risk factor for psoriatic arthropathy. The study of the combination of KIR/HLA-C receptor-ligand pairs revealed that simultaneous presence of HLA-C1 allotype did not modify the susceptibility to suffer from psoriasis observed in KIR2DL2/L2 homozygotes individuals. However, in KIR2DL2/L3 heterozygotes patients, the presence of C1 ligand had a protective effect against the disease, which in addition was dependent on the dose ligand, and independent from the presence of HLA-C*06 allele. Moreover, the combination of KIR2DS1/C2-ligand was associated specifically to type I psoriasis. The study of cytokine polymorphisms illustrated that SNPs TNF -238G>A, IL6 -174G>C and INFG +874T>A determined a higher susceptibility to psoriasis, specially type I psoriasis. However, in the case of TNF gene, the effect of the A allele could be subsidiary of a linkage disequilibrium with HLA-C*06. It was very remarkable that the association of this allele with psoriasis was present in men, but not so in women. Likewise, the IL12B -1188A>C polymorphism was associated to a modest protective effect. In conclusion, the findings of this study contribute to confirm the role of KIR/HLA-C pair and of certain cytokines such as TNF-α in the pathogenesis of psoriasis, and give us insightful hints of the importance of innate immunity in this disease.
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    Microvascular changes in relation to inflammation and epidermal hyperplasia in chronic cutaneous lesions of psoriasis vulgaris
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Výbohová, Desanka; Adamicová, Katarína; Mellová, Yvetta; Hešková, Gabriela
    Epidermal proliferation, inflammatory changes and microvascular augmentation are prominent features of chronic cutaneous psoriatic lesions. The objective of this study was the investigation of blood and lymphatic microvascular changes in relation to epidermal changes and inflammatory infiltration in dermis. Immunohistochemical analysis with antibodies to CD34, podoplanin, vascular endothelial growth factorsA and C (VEGF-A and C) and morphometric software were used for quantification of the following parameters: blood and lymphatic vessel area (BVA and LVA), VEGF-A and VEGF-C positive area, inflammatory cell infiltration in dermis (CIA) and epidermal area (EA). In comparison to healthy skin psoriatic lesions showed remarkable elevation of all measured parameters with the following average increase: BVA (2.8-times increased), LVA (2.6-times increased), VEGF-A and VEGF-C area (in epidermis 29-times and 19-times increased, in dermis 25-times and 15-times increased, respectively ), and EA (3-times increased). Statistical analysis revealed significant positive correlation between CIA and EA in psoriatic samples. Blood vessels area and VEGF-A expression in epidermis showed mild positive correlation with epidermal hyperplasia and weak positive correlation with dermal inflammatory infiltration. VEGF-A expression in epidermis also significantly correlated with blood vessels area. As for the lymphatic microcirculation we found a statistically significant positive correlation between lymphatic vessels area and the cellular infiltration in dermis but only weak correlation with epidermal hyperplasia. We hypothesize that angiogenesis in psoriasis is to a greater extent responding to epidermal hyperplasia and in a lesser way to inflammatory infiltration in dermis. However, lymphangiogenesis is significantly related to dermal inflammatory infiltration.
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    Relevance of in vitro 3-D skin models in dissecting cytokine contribution to psoriasis pathogenesis
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Chiricozzi, A.; Romanelli, M.; Panduri, S.; Donetti, E.; Prignano, F.
    Psoriasis is a chronic skin disease characterized by the activation of various T cell subsets secreting IFNγ, IL-17, and IL-22, dendritic cells producing TNFα and IFNα, and other immune cells including neutrophils and mast cells. Keratinocytes respond to different cytokine signals orchestrating innate and adaptive immune responses. In vitro studies sought to clarify the cytokine effects on keratinocytes in order to evaluate the centrality of these mediators in psoriasis pathogenesis. The aim of this review is to highlight the relevance of this peculiar in vitro approach in investigating cytokine effects on skin or multilayered epidermis. Particularly, we reported keynfinding