scholarly journals Changes in Proteome of Fibroblasts Isolated from Psoriatic Skin Lesions

2020 ◽  
Vol 21 (15) ◽  
pp. 5363
Author(s):  
Agnieszka Gęgotek ◽  
Pedro Domingues ◽  
Adam Wroński ◽  
Elżbieta Skrzydlewska
Keyword(s):  
Signal Transduction ◽  
Skin Lesions ◽  
Dermal Fibroblasts ◽  
Metabolic Effects ◽  
Psoriatic Skin ◽  
Proteomic Profile ◽  
Intercellular Signaling ◽  
Antioxidant Proteins ◽  
Skin Epidermis ◽  
Proinflammatory Factors

The dermal fibroblasts are in constant contact with the cells of the immune system and skin epidermis. Therefore, they are essential for the development of lesions in psoriasis. The aim of this study was to assess the changes in the proteomic profile of fibroblasts in the dermis of psoriasis patients, and to discuss the most significant changes and their potential consequences. The proteomic results indicate that fibroblast dysfunction arises from the upregulation of proinflammatory factors and antioxidant proteins, as well as those involved in signal transduction and participating in proteolytic processes. Moreover, downregulated proteins in psoriatic fibroblasts are mainly responsible for the transcription/translation processes, glycolysis/ adenosine triphosphate synthesis and structural molecules. These changes can directly affect intercellular signaling and promote the hyperproliferation of epidermal cells. A better understanding of the metabolic effects of the proteomic changes observed could guide the development of new pharmacotherapies for psoriasis.

scholarly journals Pellino 1 Communicates Intercellular Signaling in Chronic Skin Inflammatory Microenvironment

2018 ◽  
Author(s):  
Suhyeon Kim ◽  
Seoyoon Bae ◽  
Jihyun Park ◽  
Geun-Hyoung Ha ◽  
Kyungrim Hwang ◽  
...  
Keyword(s):  
Skin Inflammation ◽  
Skin Lesions ◽  
Psoriatic Skin ◽  
Intercellular Signaling ◽  
Multisystem Disease ◽  
Signaling Mechanism ◽  
Inflammatory Microenvironment ◽  
Systemic Signaling ◽  
Ubiquitin E3 Ligase ◽  
Chronic Skin

AbstractChronic skin inflammation including psoriasis is a multisystem disease, affecting more than 5% of the general population. Here we show that Pellino 1 (Peli1), a signal-responsive ubiquitin E3 ligase, is highly up-regulated in human psoriatic skin lesions and that increased Peli1 expression correlates with the immunopathogenesis of psoriasis-like chronic skin inflammatory disease. Interestingly, Peli1 directly interacts with interferon regulatory factor 4 (IRF4, a transcription factor that plays pivotal roles in proliferation and cytokine production) and induces lysine 63-mediated ubiquitination. Peli1-mediated IRF4 ubiquitination appears to be a common systemic signaling mechanism shared by lesional keratinocytes, dendritic cells, macrophages, and T cells, generating a feedback relationship between keratinocyte and Th17 cell responses. Conversely, inhibition of Peli1 interferes with IRF4 induction and attenuates immunopathogenic signaling in the psoriasis. In summary, Peli1-mediated ubiquitination is a common immunopathogenic intercellular signaling in psoriasis-like chronic skin inflammatory microenvironment. Thus, targeting Peli1 could be used as a potential strategy for psoriasis treatment.

Activated and cycling lymphocytes in benign dermal lymphocytic infiltrates including psoriatic skin lesions

1985 ◽  
Vol 278 (2) ◽  
pp. 92-96 ◽  
Author(s):  
G. Lange Wantzin ◽  
J. K. Larsen ◽  
I. J. Christensen ◽  
E. Ralfkiaer ◽  
M. Tjalve ◽  
...  
Keyword(s):  
Skin Lesions ◽  
Psoriatic Skin ◽  
Lymphocytic Infiltrates

Psoriatic skin lesions induced by abatacept: Case report and review of the published work

2016 ◽  
Vol 44 (7) ◽  
pp. 845-846 ◽  
Author(s):  
Ikuko Ueda-Hayakawa ◽  
Chuyen Nguyen Thi Hong ◽  
Yoko Ueki ◽  
Naotomo Kambe ◽  
Hiroyuki Okamoto
Keyword(s):  
Case Report ◽  
Skin Lesions ◽  
Psoriatic Skin

Ankylosing spondylitis, other spondyloarthritides, and related conditions

2010 ◽  
pp. 3603-3616 ◽  
Author(s):  
J. Braun ◽  
J. Sieper
Keyword(s):  
Rheumatoid Arthritis ◽  
Back Pain ◽  
Ankylosing Spondylitis ◽  
Gastrointestinal Tract ◽  
Rheumatic Diseases ◽  
Skin Lesions ◽  
Inflammatory Back Pain ◽  
Psoriatic Skin ◽  
Inflammatory Rheumatic Diseases ◽  
History Of

The spondyloarthritides are a group of inflammatory rheumatic diseases with predominant involvement of axial and peripheral joints and entheses, together with other characteristic clinical features, including inflammatory back pain, sacroiliitis, peripheral arthritis (mainly in the legs), enthesitis, dactylitis, preceding infection of the urogenital/gastrointestinal tract, psoriatic skin lesions, Crohn-like gut lesions, anterior uveitis, and a family history of Spondyloarthritis. They are the second most frequent inflammatory rheumatic diseases after rheumatoid arthritis....

scholarly journals Effects of Systemic Interleukin-10 Therapy on Psoriatic Skin Lesions: Histologic, Immunohistologic, and Molecular Biology Findings

2001 ◽  
Vol 116 (5) ◽  
pp. 721-727 ◽  
Author(s):  
Khusru Asadullah ◽  
Markus Friedrich ◽  
Sandra Hanneken ◽  
Christoph Rohrbach ◽  
Heike Audring ◽  
...  
Keyword(s):  
Molecular Biology ◽  
Skin Lesions ◽  
Interleukin 10 ◽  
Psoriatic Skin

scholarly journals Asymmetric stem-cell division ensures sustained keratinocyte hyperproliferation in psoriatic skin lesions

2015 ◽  
Vol 37 (2) ◽  
pp. 359-368 ◽  
Author(s):  
HAI-YAN JIA ◽  
YING SHI ◽  
LONG-FEI LUO ◽  
GUAN JIANG ◽  
QIONG ZHOU ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Division ◽  
Skin Lesions ◽  
Psoriatic Skin ◽  
Stem Cell Division

scholarly journals Synergistic Epithelial Responses to Endotoxin and a Naturally Occurring Muramyl Peptide

2000 ◽  
Vol 68 (3) ◽  
pp. 1235-1242 ◽  
Author(s):  
Tod A. Flak ◽  
Linda N. Heiss ◽  
Jacquelyn T. Engle ◽  
William E. Goldman
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Dna Synthesis ◽  
Metabolic Effects ◽  
Dependent Protein Kinase ◽  
Naturally Occurring ◽  
Muramyl Peptide ◽  
Dependent Protein

ABSTRACT We have investigated the synergistic interactions of a naturally occurring peptidoglycan fragment (muramyl peptide) and bacterial endotoxin in the induction of inflammatory processes within respiratory epithelial cells, at the levels of both signal transduction events and ultimate cellular metabolic effects. The source of the muramyl peptide is Bordetella pertussis, the causative agent of the respiratory disease pertussis. During log-phase growth, B. pertussis releases the muramyl peptide tracheal cytotoxin (TCT), which has the structureN - acetylglucosaminyl - 1,6 - anhydro - N - acetylmuramyl - (l) - alanyl - γ - (d) - glutamyl - meso - diaminopimelyl - (d) - alanine, equivalent to a monomeric subunit of gram-negative bacterial peptidoglycan. When applied to hamster trachea epithelial (HTE) cells, TCT and endotoxin were found to be highly synergistic in the induction of interleukin-1α (IL-1α), type II (inducible) nitric oxide synthase (iNOS), nitric oxide production, and inhibition of DNA synthesis. Neither molecule alone significantly triggered these responses. The serine/threonine protein kinase inhibitor H7 blocked induction of both IL-1α and iNOS. More selective inhibitors of protein kinase C, cyclic AMP-dependent protein kinase, and cyclic GMP-dependent protein kinase were not capable of blocking the effects of TCT and endotoxin, suggesting that the H7-inhibited component in this pathway is not among the commonly described kinase targets of H7. Treatment of HTE cells with exogenous IL-1 reproduced the induction of iNOS and DNA synthesis inhibition caused by TCT and endotoxin. H7 was not capable of interfering with effects caused by exogenous IL-1, implying that the H7-sensitive step in the pathway is upstream of IL-1 protein production. Similar assays with the phorbol ester phorbol myristate acetate indicate that it could effectively synergize with endotoxin but not with TCT, suggesting that TCT and endotoxin induce different signal transduction events that combine synergistically. The synergy observed with TCT and endotoxin in epithelial cells is significantly different from their interaction with other cell types, revealing a unique inflammatory response by epithelial cells to these natural bacterial products.

Sign in / Sign up

Export Citation Format

Share Document