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Inflammation in Skin and Joints
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Inflammation in Skin and Joints

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 6626

Special Issue Editor

Prof. Dr. Christopher Jackson

E-Mail Website
Guest Editor
Sutton Arthritis Research Laboratory, Kolling Institute, University of Sydney at Royal North Shore Hospital, Sydney, Australia
Interests: inflammation; chronic wounds; rheumatoid arthritis; skin; activated protein C; matrix metalloproteinases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The musculoskeletal system provides a framework for muscle and soft connective tissue as a support structure, whereas the skin provides an outer barrier to protect the body from environmental insults, maintain temperature, and control evaporation. Both systems play a critical role in body function and can be favourably and unfavourably affected by inflammation. There are a diverse group of musculoskeletal and skin disorders that exhibit abnormal inflammation and in some, such as psoriatic arthritis, there is a direct association between these two tissue types. Understanding the molecular mechanisms are a vital step to providing new and innovative approaches to dampen inflammation. This Special Issue calls for original research, full reviews, and perspectives that address the progress and current knowledge in the research topics of inflammatory skin and/or musculoskeletal conditions. Submissions can include any relevant work that is mechanistic in nature, such as genetic and epigenetic mechanisms; gut involvement; cell death and viability; inflammatory cytokines, mediators, receptors, and cellular signalling; innate and adaptive immune cells; connective tissue; and endothelial and epithelial cells.

Prof. Dr. Christopher Jackson
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • inflammatory skin conditions
  • inflammation in joints
  • psoriasis
  • psoriatic arthritis
  • rheumatoid arthritis
  • collagen-induced arthritis
  • dermatitis
  • barrier function
  • angiogenesis
  • keratinocytes
  • inflammatory cells
  • immune cells

Published Papers (4 papers)

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Research

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15 pages, 2561 KiB  
Article
TRPV1 Channel in Human Eosinophils: Functional Expression and Inflammatory Modulation
by Tobias Weihrauch, Natalie Gray, Daniela Wiebe, Martin Schmelz, Maren M. Limberg and Ulrike Raap
Int. J. Mol. Sci. 2024, 25(3), 1922; https://doi.org/10.3390/ijms25031922 - 05 Feb 2024
Viewed by 903
Abstract
The transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel expressed on sensory neurons and immune cells. We hypothesize that TRPV1 plays a role in human eosinophil function and is modulated by inflammatory conditions. TRPV1 expression on human eosinophils was examined [...] Read more.
The transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel expressed on sensory neurons and immune cells. We hypothesize that TRPV1 plays a role in human eosinophil function and is modulated by inflammatory conditions. TRPV1 expression on human eosinophils was examined by qPCR, flow cytometry, and immunohistochemistry, respectively. TRPV1 functionality was analyzed by investigating calcium flux, apoptosis, modulation by cytokines and acidic pH, and CD69 externalization using flow cytometry. Activation of TRPV1 induced calcium influx and prolonged survival. Although eosinophils were not directly activated by TRPV1 agonists, activation by IL-3 or GM-CSF was mainly restricted to TRPV1-positive eosinophils. TRPV1 surface content was increased by acidic pH, IL-3, IL-31, IL-33, TSLP, TNF-α, BDNF, and NGF-β. Interestingly, TRPV1 was also expressed by eosinophils located in proximity to peripheral nerves in atopic dermatitis (AD) skin. In conclusion, eosinophils express functional TRPV1 channels which are increased by extracellular acidification and AD-related cytokines. Since eosinophils also express TRPV1 in AD skin, our results indicate an important role of TRPV1 for neuroimmune interaction mechanisms in itchy, inflammatory skin diseases, like AD. Full article
(This article belongs to the Special Issue Inflammation in Skin and Joints)
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14 pages, 8197 KiB  
Article
Endothelial Protein C Receptor and 3K3A-Activated Protein C Protect Mice from Allergic Contact Dermatitis in a Contact Hypersensitivity Model
by Meilang Xue, Christopher J. Jackson, Haiyan Lin, Ruilong Zhao, Hai Po H. Liang, Hartmut Weiler, John H. Griffin and Lyn March
Int. J. Mol. Sci. 2024, 25(2), 1255; https://doi.org/10.3390/ijms25021255 - 19 Jan 2024
Viewed by 675
Abstract
Endothelial protein C receptor (EPCR) is a receptor for the natural anti-coagulant activated protein C (aPC). It mediates the anti-inflammatory and barrier-protective functions of aPC through the cleavage of protease-activated receptor (PAR)1/2. Allergic contact dermatitis is a common skin disease characterized by inflammation [...] Read more.
Endothelial protein C receptor (EPCR) is a receptor for the natural anti-coagulant activated protein C (aPC). It mediates the anti-inflammatory and barrier-protective functions of aPC through the cleavage of protease-activated receptor (PAR)1/2. Allergic contact dermatitis is a common skin disease characterized by inflammation and defective skin barrier. This study investigated the effect of EPCR and 3K3A-aPC on allergic contact dermatitis using a contact hypersensitivity (CHS) model. CHS was induced using 1-Fluoro-2,4-dinitrobenzene in EPCR-deficient (KO) and matched wild-type mice and mice treated with 3K3A-aPC, a mutant form of aPC with diminished anti-coagulant activity. Changes in clinical and histological features, cytokines, and immune cells were examined. EPCRKO mice displayed more severe CHS, with increased immune cell infiltration in the skin and higher levels of inflammatory cytokines and IgE than wild-type mice. EPCR, aPC, and PAR1/2 were expressed by the skin epidermis, with EPCR presenting almost exclusively in the basal layer. EPCRKO increased the epidermal expression of aPC and PAR1, whereas in CHS, their expression was reduced compared to wild-type mice. 3K3A-aPC reduced CHS severity in wild-type and EPCRKO mice by suppressing immune cell infiltration/activation and inflammatory cytokines. In summary, EPCRKO exacerbated CHS, whereas 3K3A-aPC could reduce the severity of CHS in both EPCRKO and wild-type mice. Full article
(This article belongs to the Special Issue Inflammation in Skin and Joints)
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Review

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17 pages, 2009 KiB  
Review
The Interaction between the Host Genome, Epigenome, and the Gut–Skin Axis Microbiome in Atopic Dermatitis
by Rodrigo Pessôa, Patricia Bianca Clissa and Sabri Saeed Sanabani
Int. J. Mol. Sci. 2023, 24(18), 14322; https://doi.org/10.3390/ijms241814322 - 20 Sep 2023
Cited by 2 | Viewed by 3112
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease that occurs in genetically predisposed individuals. It involves complex interactions among the host immune system, environmental factors (such as skin barrier dysfunction), and microbial dysbiosis. Genome-wide association studies (GWAS) have identified AD risk alleles; [...] Read more.
Atopic dermatitis (AD) is a chronic inflammatory skin disease that occurs in genetically predisposed individuals. It involves complex interactions among the host immune system, environmental factors (such as skin barrier dysfunction), and microbial dysbiosis. Genome-wide association studies (GWAS) have identified AD risk alleles; however, the associated environmental factors remain largely unknown. Recent evidence suggests that altered microbiota composition (dysbiosis) in the skin and gut may contribute to the pathogenesis of AD. Examples of environmental factors that contribute to skin barrier dysfunction and microbial dysbiosis in AD include allergens, irritants, pollution, and microbial exposure. Studies have reported alterations in the gut microbiome structure in patients with AD compared to control subjects, characterized by increased abundance of Clostridium difficile and decreased abundance of short-chain fatty acid (SCFA)-producing bacteria such as Bifidobacterium. SCFAs play a critical role in maintaining host health, and reduced SCFA production may lead to intestinal inflammation in AD patients. The specific mechanisms through which dysbiotic bacteria and their metabolites interact with the host genome and epigenome to cause autoimmunity in AD are still unknown. By understanding the combination of environmental factors, such as gut microbiota, the genetic and epigenetic determinants that are associated with the development of autoantibodies may help unravel the pathophysiology of the disease. This review aims to elucidate the interactions between the immune system, susceptibility genes, epigenetic factors, and the gut microbiome in the development of AD. Full article
(This article belongs to the Special Issue Inflammation in Skin and Joints)
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16 pages, 676 KiB  
Review
Fatigue in Inflammatory Joint Diseases
by Grzegorz Chmielewski, Michał S. Majewski, Jakub Kuna, Mateusz Mikiewicz and Magdalena Krajewska-Włodarczyk
Int. J. Mol. Sci. 2023, 24(15), 12040; https://doi.org/10.3390/ijms241512040 - 27 Jul 2023
Cited by 3 | Viewed by 1361
Abstract
Fatigue is a prevalent symptom in various rheumatic diseases, such as rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. It is characterised as a subjective, enduring feeling of generalised tiredness or exhaustion, impacting the patient’s life quality and exacerbating disability. The fatigue nature is [...] Read more.
Fatigue is a prevalent symptom in various rheumatic diseases, such as rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. It is characterised as a subjective, enduring feeling of generalised tiredness or exhaustion, impacting the patient’s life quality and exacerbating disability. The fatigue nature is multifaceted, encompassing physiological, psychological, and social factors, and although the exact cause of inflammatory joint diseases is not fully understood, several factors are believed to contribute to its development. Despite high prevalence and importance, the symptom is often underestimated in clinical practice. Chronic inflammation, commonly associated with rheumatic diseases, has been proposed as a potential contributor to fatigue development. While current treatments effectively target inflammation and reduce disease activity, fatigue remains a persistent problem. Clinical evaluation of rheumatic diseases primarily relies on objective criteria, whereas fatigue, being a subjective symptom, is solely experienced and reported by the patient. Managing fatigue in inflammatory joint diseases involves a multifaceted approach. Identifying and comprehensively assessing the subjective components of fatigue in individual patients is crucial for effectively managing this symptom in everyday clinical practice. Full article
(This article belongs to the Special Issue Inflammation in Skin and Joints)
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