Background: IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor.
Objective: To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases.
Methods: The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis.
Results: IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation. In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In vitro, staphylococcal enterotoxin B but not viruses or T(H)1 and T(H)2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside.
Conclusion: Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jaci.2005.10.033 | DOI Listing |
Biomed Rep
March 2025
Department of Biological Sciences, Sanghuh College of Life Science, Konkuk University, Seoul 05029, Republic of Korea.
Atopic dermatitis (AD) is a prevalent, persistent inflammatory skin disorder distinguished by pruritic and irritated skin. Toll-like receptors (TLRs) are specialized receptors that recognize specific patterns associated with pathogens and tissue damage, triggering an innate immune response that protects the host from invading pathogens. Previously, it was demonstrated that intradermal injection of the humanized anti-TLR2 monoclonal antibody (Ab) Tomaralimab effectively relieved AD-like skin inflammation in BALB/c mouse models exposed to house dust mite extracts.
View Article and Find Full Text PDFVet Clin North Am Small Anim Pract
December 2024
College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, 408 Raymond Stotzer Parkway, College Station, TX 77845, USA. Electronic address:
Alterations in the lipid layer and intercellular corneocyte connections can lead to increased allergen penetration through the skin surface. A normal cutaneous microbiome keeps the opportunistic pathogen Staphylococcus pseudintermedius levels low, but allergic inflammation leads to decreased diversity and increase in S pseudintermedius. Keratinocytes sound the initial allergen alarm via cytokine signaling and promote T-helper 2 (Th-2) inflammation.
View Article and Find Full Text PDFExp Dermatol
December 2024
Almirall R+D Centre, Almirall S.A, Sant Feliu de Llobregat, Spain.
Atopic dermatitis (AD) is a common inflammatory skin disorder characterised by hypersensitivity to allergens, eczematous lesions and pruritus. The aim of this study was to comprehensively characterise a murine model of dermatitis and assess the similarity with the human disease, as well as to profile clinically relevant AD therapies. Four repeated topical administrations of oxazolone in the auricular skin of sensitised mice induced morphological features compatible with AD, including redness and swelling, as well as histological changes typical of spongiotic (eczematous) dermatitis and increased plasmatic IgE.
View Article and Find Full Text PDFJ Dermatol Sci
October 2024
Juntendo Itch Research Center (JIRC), Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Urayasu, Japan; Department of Dermatology, Juntendo University Urayasu Hospital, Urayasu, Japan. Electronic address:
Background: Mechanical alloknesis (m-alloknesis) is itch hypersensitivity induced by normally innocuous stimuli. It is sometimes observed in dry skin based itch-related diseases such as atopic dermatitis (AD), and often triggers the vicious itch-scratch cycle. The acetone-ether and water (AEW) mouse model mimics dry skin-induced m-alloknesis, yet its underlying mechanism remains unclear.
View Article and Find Full Text PDFCytokine
January 2025
Department of Allergy, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Institute of Allergy and Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.. Electronic address:
Background: Omalizumab, an anti-IgE biological agent, is commonly prescribed as a second-line therapy for Chronic Spontaneous Urticaria (CSU). However, there is a lack of biomarkers to predict which CSU patients will respond favorably to omalizumab.
Objective: Our study aims to identify cytokine markers associated with the efficacy of omalizumab in treating CSU.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!