The suppression of dermatitis by combined therapy was accompanied

The suppression of dermatitis by combined therapy was accompanied by a decrease in the plasma level of IgE and in the splenic level of IL-5, IL-13, TARC and eotaxin. Histological finding indicated that the dermal infiltration of inflammatory cells including mast cells and eosinophils was greatly reduced. Particularly, immunohistological evaluation reveals a reduction in CD3+ T cells and CLA+ cells in the combined therapy. Our findings suggest that combination therapy of glucosamine plus FK-506 was more synergistic efficacy than single-modality treatment with either

alone to improve the development of established dermatitis in NC/Nga mice model. This combined immunosuppressive therapy may provide an effective therapeutic strategy for the treatment of AD. Atopic dermatitis selleck inhibitor (AD), or atopic eczema, is a common, chronic, inflammatory skin disease [1, 2]. The worldwide lifetime prevalence of AD in children is 10–20%, and in adults it is 1–3% [3]. Several

lines of evidence suggest the contribution of immunological mechanisms in the pathogenesis of Compound Library manufacturer AD. Several immunology reports have suggested T-helper 1 (Th1)/T-helper 2 (Th2) imbalance in AD [4, 5]. This imbalance favours Th2, and high serum immunoglobulin (Ig) E levels as well as infiltration with immune cells such as eosinophils, mast cells and cutaneous lymphocyte antigen (CLA) T cells [6–8], which are all characteristics of AD, are provoked by Th2 cytokines, interleukin-4 (IL-4), IL-5 and IL-13 [9]. Patients with AD show elevated plasma IgE levels in response to many kinds of allergens, while keratinocytes of patients

with AD exhibit the propensity to produce exaggerated amounts of cytokines, a phenomenon that can play a major role in the promotion Adenosine triphosphate and maintenance of inflammation [10, 11]. Glucosamine is a common constituent of the glycosaminoglycans in the cartilage matrix and synovial fluid. Use of glucosamine is common in patients with osteoarthritis, because of its pharmacological effects on articular cartilage and joint tissue [12, 13]. In fact, its anti-inflammatory activity may allow for reduced doses of non-steroidal anti-inflammatory agents. The suppression of inflammatory activity may result from the potential immunoregulatory capability of glucosamine. It has been reported that glucosamine suppresses proliferation and differentiation of unprimed CD4+ T cells and is more inhibitory towards the development of Th2-mediated immune responses than Th1-mediated immune responses [14]. Thus, glucosamine has immunosuppressive properties also [15]. We recently reported that prophylactic treatment with glucosamine improved clinical symptoms in Dermatophagoides farinae (Df)-induced NC/Nga mice, with reduced infiltration of mast cells and eosinophils into skin, and that it selectively suppressed Th2-mediated immune responses [16].

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