Article

Mast cells in atopic dermatitis

Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Current opinion in immunology (Impact Factor: 7.48). 10/2009; 21(6):666-78. DOI: 10.1016/j.coi.2009.09.006
Source: PubMed

ABSTRACT

Mast cells play as the major effector cells in immediate hypersensitivity through activation via the high-affinity IgE receptor, Fc epsilon RI, although many other functions have recently been discovered for this cell type. Given the broad array of proinflammatory mediators secreted from Fc epsilon RI-activated mast cells, as well as sensitization to allergens, IgE elevation, and increased mast cells in a majority of atopic dermatitis patients, mast cells are believed to be involved in the pathogenesis of atopic dermatitis. Numerous animal models have been used to study this epidemic disease. Here we review the recent progress to synthesize our current understanding of this disease and potential mechanisms for a mast cell's role in the disease.

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Available from: Toshiaki Kawakami, Dec 19, 2013
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    • "Mast cell activation leads to different cellular processes beyond degranulation. Different cytokines and chemokines are produced by mast cells depending on the activation signal (Kawakami et al., 2009). TNF-␣ is a well-known cytokine that mast cells can release from preformed storage or produce de novo after infection with different pathogens (St John and Abraham, 2013). "
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    ABSTRACT: Mast cells are crucial elements of the innate immune response. They reside in tissues that are commonly exposed to the external environment, such as the skin and mucosae, where they can rapidly detect the presence of pathogens and mount a potent inflammatory response that recruits other cellular effectors of the immune response. The contribution of mast cells to the immune response to viruses, bacteria, protozoa and multicellular parasites is well established, but there is scarce information about the role of these cells in fungal infections. In this study, we analyzed if mast cells are activated by Candida albicans and if the C-type lectin receptor Dectin-1 is involved in its recognition. We found that both yeasts and hyphae of C. albicans-induced mast cell degranulation and production of TNF-α, IL-6, IL-10, CCL3 and CCL4, while only yeasts were able to induce IL-1β. Mast cells also produced ROS after stimulation with both dimorphic phases of C. albicans. When mast cells were activated with yeasts and hyphae, they showed decreased expression of IκBα and increased presence of phosphorylated Syk. Blockade of the receptor Dectin-1, but not Toll-like receptor 2, decreased TNF-α production by mast cell in response to C. albicans. These results indicate that mast cells are capable of sensing the two phases of C. albicans, and suggest that mast cells participate as an early inductor of inflammation during the early innate immune response to this fungus. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Full-text · Article · May 2015 · Immunobiology
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    • "Mast cells are widely distributed through several mammalian tissues including blood vessels, the central nerve system (CNS), epithelium and smooth muscle (Busse and Mathur, 2010). These cells have been shown to regulate the protection of immune responses to some parasites and bacteria, as well as IgE-mediated immediate hypersensitivity and allergic disorders (Kawakami et al., 2009; Galli, 2000). Similarly, numbers of mast cell were detected in young (6 weeks) and old (3-12 months) C57BL/6 mice (Nguyen et al., 2005). "

    Preview · Article · Jan 2015 · Archives of Biological Sciences
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    • "For personal use only. increase in the mast cell number (Kawakami et al., 2009). Therapeutic agents for AD can affect mast cells number. "
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    ABSTRACT: Atopic dermatitis (AD) is a chronic and relapsing skin disease with severe eczematous lesions. Long-term topical corticosteroid treatment can induce skin atrophy, hypopigmentation and transepidermal water loss (TEWL) increase. A new treatment approach was needed to reduce the risk by dermal targeting. For this purpose, Betamethasone valerate (BMV)/Diflucortolone valerate (DFV)-loaded liposomes (220–350 nm) were prepared and incorporated into chitosan gel to obtain adequate viscosity (∼13 000 cps). Drugs were localized in stratum corneum + epidermis of rat skin in ex-vivo permeation studies. The toxicity was assessed on human fibroblast cells. In point of in-vivo studies, pharmacodynamic responses, treatment efficacy and skin irritation were evaluated and compared with previously prepared nanoparticles. Liposome/nanoparticle in gel formulations produced higher paw edema inhibition in rats with respect to the commercial cream. Similar skin blanching effect with commercial creams was obtained via liposome in gels although they contain 10 times less drug. Dermatological scoring results, prognostic histological parameters and suppression of mast cell numbers showed higher treatment efficiency of liposome/nanoparticle in gel formulations in AD-induced rats. TEWL and erythema measurements confirmed these results. Overview of obtained results showed that liposomes might be an effective and safe carrier for corticosteroids in skin disease treatment.
    Full-text · Article · Sep 2014 · Drug Delivery
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