Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data on skin reactivity in patients with respiratory atopy without atopic dermatitis are scarce and controversial. Our purpose was to assess whether skin reactivity in patients with seasonal allergic rhinitis varies according to the phase of the disease and the possible release of inflammatory mediators acting on the skin during the pollen season. The volar forearm skin of eleven patients with seasonal allergic rhinitis without atopic dermatitis was challenged with a single exposure to sodium lauryl sulfate. The skin response was evaluated instrumentally over 72 h by transepidermal water loss, capacitance and echogenicity measurements for the assessment of skin damage and the inflammatory response. Tests were performed in winter and repeated in spring in seasonal allergic rhinitis patients, when they showed respiratory symptoms. Fifteen subjects with atopic dermatitis underwent the same experimental procedure in winter as a control population. Baseline and postexposure values were similar both in winter and in spring in seasonal allergic rhinitis patients. After sodium lauryl sulfate challenge, atopic dermatitis patients showed a higher degree of skin barrier damage and inflammation compared to patients with seasonal allergic rhinitis. These findings suggest that subjects with seasonal allergic rhinitis without atopic dermatitis have normal epidermal barrier function and normal skin reactivity during both the inactive and the active phase of the disease. Inflammatory mediators possibly released by mucous membranes during active allergic rhinitis do not influence skin barrier function.
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PMID:No increased skin reactivity in subjects with allergic rhinitis during the active phase of the disease. 1095 10

Interleukin-31 (IL-31) is a type 2 helper T-cell-derived cytokine that has recently been shown to cause severe inflammation and tissue remodeling in multiple chronic diseases of the skin and lungs. IL-31 is upregulated in allergic and inflammatory diseases, including atopic dermatitis, asthma, cutaneous T-cell lymphomas, and allergic rhinitis, as well as autoimmune diseases such as systemic erythematosus. Overexpression of IL-31 in T cells causes severe inflammation, with histological features similar to skin lesions of patients with atopic dermatitis. However, the molecular mechanisms involved in IL31-driven pathological remodeling in skin diseases remain largely unknown. Here, we studied the role of IL-31 in skin damage as a result of intradermal administration of recombinant IL-31 into mice. Notably, IL-31 was sufficient to increase epidermal basal-cell proliferation and thickening of the epidermal skin layer. Our findings demonstrate a progressive increase in transepidermal water loss with chronic administration of IL-31 into the skin. Further, analysis of the skin transcriptome indicates a significant increase in the transcripts involved in epidermal-cell proliferation, epidermal thickening, and mechanical integrity. In summary, our findings demonstrate an important role for IL-31 signaling in epidermal cell proliferation and thickening that together may lead to impaired skin-barrier function in pathological remodeling of the skin.
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PMID:IL-31-Driven Skin Remodeling Involves Epidermal Cell Proliferation and Thickening That Lead to Impaired Skin-Barrier Function. 2811 22