**5. Atopic dermatitis (AD): Physiopathology of AD**

Atopic dermatitis or atopic eczema (AD/AE) is a chronic inflammatory disease of the skin, which usually occurs in the early years of life. The skin in AD is extremely dry and itchy and is inflamed - this leads to the characteristic redness, swelling, and scaling pattern often seen in the face and at flexural surfaces of the extremities of patients suffering from AD. AD has been divided in at least 2 different forms: (i) IgE associated or extrinsic dermatitis; (ii) non-IgE associated or intrinsic dermatitis.

Based on epidemiological and immunological studies, the natural history of AD seems to follow three phases: an initial non-atopic (non-IgE associated) form of eczema occurring in the early infancy followed in 60 to 80% of the cases by a sensitization to food and /or environmental allergens with the development of associated IgE (true AD). Finally, an IgE sensitization to self-proteins is observed in a high proportion of children and adults with AD due to molecular mimicry (Bieber, 2008).

AD is often the first disorder to manifest in the relay of allergies, usually referred to as the Atopic March (Hahn and Bacharier, 2005; Illi et al., 2004; Spergel and Paller, 2003; Zheng et al., 2011). The prevalence of the disorder has increased dramatically in the last two decades similar to other allergies such as allergic rhinitis and asthma. AD affects mostly infants and young children and according to recent epidemiological studies, 5-20% of

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children are affected in developed countries (Asher et al., 2006; Williams et al., 1999). The treatment of AD is mainly symptomatic and includes emollients to moisturize the skin, and topical corticosteroids along with a switch to an elimination diet (BuBmann et al., 2009; Peserico et al., 2008).

AD has a complex etiology. Recent investigations into mechanisms that drive the inflammatory response in AD have highlighted the crucial role of genetic predisposition. Many mutations have been associated to the development of AD. These mutations are located in two subsets of genes, in structural protein genes involved in the epidermal-barrier function or in genes involved in IgE production (Bieber, 2008; Demehri et al., 2009; Hsu et al., 2008; Suzuki et al., 2011). Also, environmental factors can contribute to the development of AD. As such, AD can be classified into IgE-mediated and non IgE-mediated subtypes (Fig. 1.).

As mentioned above, it has been postulated ("hygiene hypothesis") that the pattern of bacterial colonization of the gut during the early months after birth can contribute to the development of AD (Vael and Desager, 2009). During the first year of life the newborn immune system is still under development while exposure to novel dietary foods is increasing, especially around the weaning period. These multifactorial events in concert contribute to the establishment of oral tolerance, *i.e.* prevention or development of atopic sensitization to common foods such as cow's milk, eggs, wheat and nuts that predispose to the development of AD (Garcia et al., 2007; Gonzalez, I et al., 1971; Han et al., 2004; Heratizadeh et al., 2011).
