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Daejeon, South Korea

Lee S.E.,Yonsei University | Jeong S.K.,Neopharm Co. | Lee S.H.,Yonsei University
Yonsei Medical Journal | Year: 2010

Proteases in the skin are essential to epidermal permeability barrier homeostasis. In addition to their direct proteolytic effects, certain proteases signal to cells by activating protease-activated receptors (PARs), the G-protein-coupled receptors. The expression of functional PAR-2 on human skin and its role in inflammation, pruritus, and skin barrier homeostasis have been demonstrated. Atopic dermatitis (AD) is a multifactorial inflammatory skin disease characterized by genetic barrier defects and allergic inflammation, which is sustained by gene-environmental interactions. Recent studies have revealed aberrant expression and activation of serine proteases and PAR-2 in the lesional skin of AD patients. The imbalance between proteases and protease inhibitors associated with genetic defects in the protease/protease inhibitor encoding genes, increase in skin surface pH, and exposure to proteolytically active allergens contribute to this aberrant protease/ PAR-2 signaling in AD. The increased protease activity in AD leads to abnormal desquamation, degradation of lipid-processing enzymes and antimicrobial peptides, and activation of primary cytokines, thereby leading to permeability barrier dysfunction, inflammation, and defects in the antimicrobial barrier. Moreover, up-regulated proteases stimulate PAR-2 in lesional skin of AD and lead to the production of cytokines and chemokines involved in inflammation and immune responses, itching sensation, and sustained epidermal barrier perturbation with easier allergen penetration. In addition, PAR-2 is an important sensor for exogenous danger molecules, such as exogenous proteases from various allergens, and plays an important role in AD pathogenesis. Together, these findings suggest that protease activity or PAR-2 may be a future target for therapeutic intervention for the treatment of AD. © Yonsei University College of Medicine 2010.

Kim H.-J.,University of Ulsan | Kim Y.-J.,University of Ulsan | Lee S.-H.,University of Ulsan | Yu J.,University of Ulsan | And 2 more authors.
Clinical Immunology | Year: 2014

Allergic march (AM) is characterized by the progression of clinical signs of atopic dermatitis (AD) to allergic asthma or rhinitis, but its pathogenesis is not completely understood.We developed mouse model of AM with three 1-week exposures (separated by 2-week interval) to an OVA or saline (control) followed by OVA challenge. The development of AM was confirmed by phenotypes of AD and allergic asthma. Increases in IL-4, IL-17, and thymic stromal lymphopoietin (TSLP) responses were associated with the progression of AM, and these responses were suppressed by treatment with Lcr35. Moreover, Lcr35 treatment led to an increase in the number of CD4+CD25+ Foxp3+ regulatory T (Treg) cells in the mesenteric lymph nodes (MLNs) of AM mice.In conclusion, the oral application of Lcr35 prevented the development of AM in this model by suppressing Th2, Th17, and TSLP responses via a mechanism that may involve CD4+CD25+Foxp3+ Tregs in MLNs. © 2014 Elsevier Inc.

Provided are a composition and an external application for promoting muscle differentiation or improving muscle mass containing an amino acid derivative promoting muscle cell differentiation, a composition and an external application for alleviating muscle function deterioration caused by muscle damage and recovering damaged muscle containing the same, or a pharmaceutical composition and an external application for treating or improving a muscle deterioration disease containing the same.

Provided are heterocyclic compounds, having effects of treating and preventing inflammatory diseases and treating skin wounds, and particularly, exhibiting effects of recovering disrupted skin barriers, mitigating inflammation, and pruritus. Also, a composition containing the compound as an effective component can be used to mitigate various inflammatory diseases and protease activated receptor-2 (PAR-2)-overexpressed diseases, and can be particularly used as a composition having an anti-inflammatory function in inflammatory skin diseases including atopic dermatitis and the like, by inhibiting PAR-2 activity.

Disclosed is a compound having an acceleration effect on the secretion of human -defensin, LL-37, which is a human-derived anti-microbial peptide, a method for preparing same, and a composition for accelerating the secretion of anti-microbial peptide having same as an active ingredient, and the compound and the composition using same of the present invention enhance the anti-microbial effect and the immunity control effect that the anti-microbial peptide has in the body by accelerating the secretion of the anti-microbial peptide in the body.

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