ABSTRACT
Atopic dermatitis (AD) is a pruritic in™ammatory skin disease associated with a personal or family history of allergy. AD can occur at any age; most often it affects infants and young children. In some instances, it may persist into adulthood or actually ’rst show up later in life. The prevalence of AD is on the rise and estimated at ~17% in the United States. The fundamental lesion in AD is a defective barrier that results in dry, itchy skin, and is aggravated by mechanical injury in™icted by scratching. This allows entry of antigens via the skin and creates a milieu that shapes the immune response to these antigens (Oyoshi et al., 2009). Clinical observations suggest that AD is the cutaneous manifestation of a systemic disorder that gives rise to asthma, food allergy, and allergic rhinitis (Novak and Bieber, 2003). This in™ammatory disorder is exclusively characterized by elevated serum IgE levels and peripheral eosinophilia. At the molecular level, AD is categorized into two types: extrinsic, which involves IgE-dependent sensitization and makes up to 70-80% of the patients, and intrinsic, which involves IgE-mediated sensitization and makes up 20-30% of the patients worldwide (Novak and Bieber, 2003). Both forms of AD have associated eosinophilia. In extrinsic AD, memory T cells expressing the skin homing receptor, cutaneous lymphocyte-associated antigen (CLA), produce increased levels of Th2 cytokines. These include IL-4 and IL-13, which are known to induce isotype switching to IgE synthesis, as well as IL-5, which plays an important role in eosinophil development and survival. These CLA+ T cells also produce abnormally low levels of IFN-γ, a Th1 cytokine known to inhibit Th2 cell function. Intrinsic AD is associated with less IL-4 and IL-13 production than extrinsic AD (Leung et al., 2004). On the whole, AD is considered one of the common, often
20.1 Introduction .......................................................................................................................... 257 20.2 Phloroglucinol Derivatives and Their Possible Role in the Treatment of AD ...................... 259 20.3 Fucoidans and Their Possible Role in the Treatment of AD ................................................ 262 20.4 Conclusions and Future Prospects ........................................................................................264 References ......................................................................................................................................264
