scholarly journals PSORIASIS IN HIV-INFECTED PATIENTS: CLINICAL AND LABORATORY EVALUATION, APPROACHES TO THERAPY

2017 ◽  
Vol 20 (4) ◽  
pp. 227-231
Author(s):  
Evgeny Yu. Evdokimov ◽  
A. V Sundukov
Keyword(s):  
Practical Interest ◽  
Skin Lesions ◽  
Laboratory Evaluation ◽  
Psoriatic Skin ◽  
Inflammatory Reactions ◽  
Treatment Regimens ◽  
Before And After ◽  
Index Of Severity ◽  
Evaluation Approaches

Clinical and laboratory evaluation of the effectiveness of therapy of psoriasis vulgaris in 78 HIV-infected patients using the two treatment regimens is presented. Peculiarities of clinical course of psoriasis depending on the number of CD4+lymphocytes in the peripheral blood are shown. Histological and histochemical studies of biopsy samples from psoriatic skin lesions and apparently healthy skin in 15 people were performed. The dynamics before and after treatment of CD4+ and CD8+ lymphocytes in biopsies of skin and blood, their relationship with the index of severity of psoriasis (PASI) are presented. This study is of theoretical and practical interest in understanding the value and role of CD4+ and CD8+ lymphocytes in the formation of inflammatory reactions in the skin of patients with psoriasis as a possible option for treatment of psoriasis in HIV-infected patients.

The role of telomerase activity in psoriatic skin lesions

2007 ◽  
Vol 68 (5) ◽  
pp. 1093-1095 ◽  
Author(s):  
Davor Jurisic ◽  
Ivan Kirin ◽  
Domagoj Rabic ◽  
Bojan Dojcinovic ◽  
Miran Coklo ◽  
...  
Keyword(s):  
Skin Lesions ◽  
Telomerase Activity ◽  
Psoriatic Skin

scholarly journals Interleukin 17 Expression in Psoriatic Skin Lesions before and after Treatment with Platelet Rich Plasma (PrP)

2018 ◽  
Vol 86 (6) ◽  
pp. 1447-1456
Author(s):  
ENAS S. MOHAMMED, M.Sc.; MONA A. ATWA, M.D. ◽  
SAHAR F. MANSOUR, M.D.; NADER A. ISMAIL, M.D.
Keyword(s):  
Platelet Rich Plasma ◽  
Skin Lesions ◽  
Psoriatic Skin ◽  
Interleukin 17 ◽  
Before And After

scholarly journals miR-155 Contributes to Normal Keratinocyte Differentiation and Is Upregulated in the Epidermis of Psoriatic Skin Lesions

2020 ◽  
Vol 21 (23) ◽  
pp. 9288
Author(s):  
Lucian Beer ◽  
Polina Kalinina ◽  
Martin Köcher ◽  
Maria Laggner ◽  
Markus Jeitler ◽  
...  
Keyword(s):  
Skin Diseases ◽  
Normal Skin ◽  
Skin Lesions ◽  
Keratinocyte Differentiation ◽  
Psoriatic Skin ◽  
Bioinformatics Analyses ◽  
Epidermal Barrier ◽  
Barrier Formation

The role of microRNAs (miRNAs) during keratinocyte (KC) differentiation and in skin diseases with epidermal phenotypes has attracted strong interest over the past few years. However, combined mRNA and miRNA expression analyses to elucidate the intricate mRNA–miRNA networks of KCs at different stages of differentiation have not been performed yet. In the present study, we investigated the dynamics of miRNA and mRNA expression during KC differentiation in vitro and in normal and psoriatic epidermis. While we identified comparable numbers of up- and downregulated mRNAs (49% and 51%, respectively), miRNAs were predominantly upregulated (76% vs 24%) during KC differentiation. Further bioinformatics analyses suggested an important inhibitory role for miR-155 in KC differentiation, as it was repressed during KC differentiation in normal skin but strongly upregulated in the epidermis of psoriatic skin lesions. Mimicking the inflammatory milieu of psoriatic skin in vitro, we could show that the pro-inflammatory cytokines IL17, IL1β and INFγ synergistically upregulated miR-155 expression in KCs. Forced over-expression of miR-155 in human in vitro skin models specifically reduced the expression of loricrin (LOR) in KCs, indicating that miR-155 interferes with the establishment of a normal epidermal barrier. Together, our data indicate that downregulation of miR-155 during KC differentiation is a crucial step for epidermal barrier formation. Furthermore, its strong upregulation in psoriatic lesions suggests a contributing role of miR-155 in the altered keratinocyte differentiation observed in psoriasis. Therefore, miR-155 represents as a potential target for treating psoriatic skin lesions.

scholarly journals RNA-antimicrobial peptide LL-37 complexes fuel a TLR- and NET-mediated inflammatory cycle of neutrophil activation in psoriasis

2018 ◽  
Author(s):  
Franziska Herster ◽  
Zsofia Bittner ◽  
Sabine Dickhöfer ◽  
David Eise ◽  
Tatjana Eigenbrod ◽  
...  
Keyword(s):  
Antimicrobial Peptide ◽  
Intervention Strategy ◽  
Skin Lesions ◽  
Neutrophil Extracellular Trap ◽  
Psoriatic Skin ◽  
Bacterial Rna ◽  
Human Pmns ◽  
Inflammatory Autoimmune Disease

AbstractPsoriasis is an inflammatory autoimmune disease characterized by skin lesions showing strong neutrophil (PMN) infiltration and high levels of the antimicrobial peptide, LL37, but the role of PMNs in this context remains unclear. We here show that primary human PMNs, especially PMNs from psoriasis patients, not only respond via TLR8 to human and bacterial RNA in complexed with LL37 by cytokine-, chemokine- and neutrophil extracellular trap (NET)-release; they also actively release additional RNA and LL37 in response to stimulation by the same complex and both RNA and LL37 were found to be highly abundant in psoriatic skin. Moreover, RNA-LL37-induced NETs propagated PMN activation and could thus fuel a PMN-mediated and self-sustaining inflammatory loop that may represent an unexpected early initiator or amplifying event in psoriasis. Given that TLR inhibitory oligodeoxynucleotides prevented the cytokine production and NETosis of PMNs by RNA-LL37 complexes in vitro, our study also highlights TLR blockade as a potential therapeutic intervention strategy in psoriasis.SummaryHuman and bacterial RNA in complex with LL37 activates neutrophils via TLR8 to release cytokines, chemokines and neutrophil extracellular traps (NETs). NETs and neutrophil-rich areas in psoriatic skin contain RNA and LL37, suggesting RNA-LL37 may fuel a PMN-mediated and self-sustaining inflammatory cycle in psoriasis.

Cyclin D1, B and A expression and cell turnover in psoriatic skin lesions before and after cyclosporin treatment

2000 ◽  
Vol 143 (5) ◽  
pp. 950-956 ◽  
Author(s):  
C. Miracco ◽  
M. Pellegrino ◽  
M.L. Flori ◽  
R. Vatti ◽  
M. Materno ◽  
...  
Keyword(s):  
Cyclin D1 ◽  
Skin Lesions ◽  
Psoriatic Skin ◽  
Cell Turnover ◽  
Cyclosporin Treatment ◽  
Before And After

scholarly journals Interleukin-17A blockade with secukinumab results in decreased neutrophil infiltration in psoriasis: minimally-invasive measurement by tape stripping

2016 ◽  
Vol 1 (1) ◽  
Author(s):  
Christian Loesche ◽  
Frank Kolbinger ◽  
Marie-Anne Valentin ◽  
Philip Jarvis ◽  
Melanie Ceci ◽  
...  
Keyword(s):  
Minimally Invasive ◽  
Immunohistochemical Analysis ◽  
Neutrophil Infiltration ◽  
Skin Lesions ◽  
Psoriatic Skin ◽  
Tape Stripping ◽  
Neutrophil Accumulation ◽  
Interleukin 17A ◽  
Before And After ◽  
Invasive Method

Psoriasis is a well characterized interleukin (IL)-17A-driven skin disease with neutrophil infiltration and epidermal hyperkeratosis. Several biomarkers, most prominently β-defensin-2 (BD-2), have been identified using local and systemic invasive measurements as responsive markers of IL-17A-driven skin pathology. We sought to determine whether measurements of epidermal proteins by tape stripping could offer a minimally-invasive method to assess treatment responses. We compared the expression of 170 proteins in the epidermis (tape stripping) and dermis (open flow microperfusion) of 8 psoriatic subjects before and after administration of a single dose of subcutaneous (s.c.) antiIL-17A mAb secukinumab. Proteomic analyses of tape strips revealed a >3-fold decrease in 32 epidermal and inflammatory cell proteins in response to secukinumab. The epidermal proteins with the largest (>10-fold) decreases were: matrix metalloproteinase-8 (MMP-8, 15.68-fold, p<0.05); myeloperoxidase (MPO, 14.72-fold, p<0.005); IL-8 (11.93-fold, p<0.05); MMP-9 (10.81-fold, p<0.005); and IL-1β (10.35-fold, p<0.05). For these proteins, greater-fold protein changes were detected in the epidermis compared to dermis. Immunohistochemical analysis confirmed that neutrophils are the predominant cell type in psoriatic skin lesions that express MPO, MMP-8 and MMP-9, and that secukinumab treatment dramatically decreases neutrophil accumulation. Thus, tape stripping may be used to assess epidermal neutrophils, and protein biomarker responses to anti-IL-17A therapy in psoriasis.

scholarly journals The role of mixed Mycoplasma and Herpesvirus infections in case of skin lesions in children

2019 ◽  
Vol 18 (3) ◽  
pp. 5-10
Author(s):  
H. O. Kuvardina ◽  
F. S. Kharlamova ◽  
I. V. Polesko ◽  
O. V. Shamsheva ◽  
O. S. Ostapuschenko
Keyword(s):  
Skin Diseases ◽  
Skin Lesions ◽  
Stevens Johnson Syndrome ◽  
Vascular Endothelial ◽  
Herpesvirus Infection ◽  
Inflammatory Reactions ◽  
Immune Mediated ◽  
Johnson Syndrome ◽  
Allergic Skin

Numerous literature data show the role of mycoplasma infection in the development of non-respiratory lesions of various organs and systems, including the skin. Herpesvirus and mycoplasma infections can trigger the development of immune-mediated inflammatory reactions of the skin and mucous membranes — erythema multiforme exudative, Stevens-Johnson syndrome, vesicular pustular dermatosis — Sneddon-Wilkinson syndrome, etc.In order to study the frequency and nature of skin lesions with mycoplasmosis combined with herpesvirus infection, 45 patients aged 3 to 15 years of life were observed. A comprehensive clinical and laboratory study revealed skin lesions in 27 patients associated with current mycoplasma and herpesvirus infections. Thus, multiforme exudative erythema in the small form variant was diagnosed in 13 patients, skin vasculitis in 4, hemorrhagic purpura in 3, urticaria rash in 3, erythema nodosum in 2, mucositis in 2 children. In 18 children, a combined mycoplasma and herpesvirus infection was established. In 9 children, a mono infection was detected (in 5 — herpes virus and in 4 — mycoplasma).All observed patients showed antibodies to smooth muscle antigens in titers from 1:80 to 1:160 (normal 1:40) and in the vast majority (in 24 patients) — antibodies to vascular endothelial antigens in titers from 1:80 to 1:320 (with the norm of 1:40). Compaction of the intima-media complex was detected in 6 patients with monoinfection and in 16 patients with co-infection, according to ultrasound duplex scanning of the vessels of the brachiocephalic department.Thus, for various immuno-inflammatory, allergic skin diseases, screening for infections, in particular, mycoplasma and herpesvirus, is necessary to optimize treatment.

scholarly journals Purinergic Signaling and Inflammasome Activation in Psoriasis Pathogenesis

2021 ◽  
Vol 22 (17) ◽  
pp. 9449
Author(s):  
Davide Ferrari ◽  
Fabio Casciano ◽  
Paola Secchiero ◽  
Eva Reali
Keyword(s):  
T Cell Activation ◽  
Cell Activation ◽  
Purinergic Signaling ◽  
Critical Role ◽  
Clinical Manifestations ◽  
Skin Lesions ◽  
Psoriatic Skin ◽  
Inflammasome Activation ◽  
Increased Risk

Psoriasis is a chronic inflammatory disease of the skin associated with systemic and joint manifestations and accompanied by comorbidities, such as metabolic syndrome and increased risk of cardiovascular disease. Psoriasis has a strong genetic basis, but exacerbation requires additional signals that are still largely unknown. The clinical manifestations involve the interplay between dendritic and T cells in the dermis to generate a self-sustaining inflammatory loop around the TNFα/IL-23/IL-17 axis that forms the psoriatic plaque. In addition, in recent years, a critical role of keratinocytes in establishing the interplay that leads to psoriatic plaques’ formation has re-emerged. In this review, we analyze the most recent evidence of the role of keratinocytes and danger associates molecular patterns, such as extracellular ATP in the generation of psoriatic skin lesions. Particular attention will be given to purinergic signaling in inflammasome activation and in the initiation of psoriasis. In this phase, keratinocytes’ inflammasome may trigger early inflammatory pathways involving IL-1β production, to elicit the subsequent cascade of events that leads to dendritic and T cell activation. Since psoriasis is likely triggered by skin-damaging events and trauma, we can envisage that intracellular ATP, released by damaged cells, may play a role in triggering the inflammatory response underlying the pathogenesis of the disease by activating the inflammasome. Therefore, purinergic signaling in the skin could represent a new and early step of psoriasis; thus, opening the possibility to target single molecular actors of the purinome to develop new psoriasis treatments.

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