Preface

Atopic Dermatitis is a common disease characterized by inflamed, itching and dry skin. This relapsing allergic disorder has complex etiology and shows a remarkably high clinical heterogeneity which complicates the diagnosis and clinical management.

This book is divided into 4 sections. The first section (Disease Etiology) describes some of the physiological mechanisms underlying Atopic Dermatitis, including alterations in the immune system and the skin-barrier function. The important role of host-microorganism interactions on the pathophysiology of Atopic Dermatitis is discussed in the second section (Microorganisms in Atopic Dermatitis). An overview of the clinical diagnostic criteria and the disease management protocols commonly used is given in the third section (Diagnosis and Clinical Management). The last section (New Treatments) describes new therapeutic approaches that are not widely used but are currently being studied due to preliminary evidence showing a clinical benefit for Atopic Dermatitis.

As a co-editor, it was my greatest pleasure to work with Dr Jorge Esparza-Gordillo on this book, which handles cutting-edge ideas on atopic dermatitis, provided by ambitious specialists. Every chapter is a real pearl of the subject, and as a clinicianscientist, I was delighted to read the manuscript one by one. I believe clinicians and researchers worldwide will benefit from this book as a unique free online publication.

Thanks to Ms. Bojana Zelenika and Mr. Dejan Grgur of InTech - Open Access Publisher, this book is published with a very quick publication process, and will thus reach the reader with the latest information. Last but not least, I thank my wife Shoko for her enormous support during this project.

> **Itaru Dekio, MD, PhD**  Department of Dermatology, Faculty of Medicine, Shimane University, Izumo, Japan

**Part 1** 

**Disease Etiology** 

**Part 1** 

**Disease Etiology** 

**1** 

*Japan* 

**Flaky Tail Mouse as a Novel Animal Model of** 

 **in the Development of Atopic Dermatitis** 

*Department of Dermatology, Kyoto University Graduate School of Medicine* 

Catharina Sagita Moniaga and Kenji Kabashima

**Atopic Dermatitis: Possible Roles of Filaggrin** 

Understanding of human diseases has been enormously expanded by the use of animal models, because they allow for in-depth investigation of pathogenesis and provide invaluable tools for diagnostic and pharmaceutical purposes. Atopic dermatitis (AD) is a chronic, relapsing form of skin inflammation, a disturbance of epidermal-barrier function that culminates in dry skin, pruritus, and IgE-mediated sensitization to food and environmental allergens (Bieber, 2008, Mori, et al., 2010, Tokura, 2010). AD is a common disease with no satisfactory form of therapy; therefore, understanding the mechanism of AD through animal models is an urgent issue to be solved (Jin, et al., 2009, Matsuda, et al., 1997, Shiohara, et al., 2004). The complexity and variability of AD and multiple genetic and environmental factors underlying AD make creating a reproducible, accessible, and relevant

Thus far, a number of mouse models have been developed. These models can be categorized into three groups: (1) models induced by epicutaneous application of sensitizers; (2) transgenic mice that either overexpress or lack selective molecules; and (3) mice that spontaneously develop AD-like skin lesions. These models display many features of human AD, and their studies have resulted in a better understanding of the pathogenesis of AD. They allow for an in-depth dissection of the mediators and cells that are critical for the

Located at the interface between the body and the environment, the epidermis is an elaborate structure that shares few properties with other biological barriers. Key functions include providing physical and biochemical protection (O'Regan &Irvine, 2010), and playing important roles in host defense, inflammation, and regulation of immune responses (Schleimer, et al., 2007). Patients with AD exhibit impaired skin barrier functions and abnormal structure and chemistry of the stratum corneum (SC) (Leung &Bieber, 2003). Alteration of the skin barrier in AD is evidenced by reduction in the water content of the SC and by increased transepidermal water loss (TEWL) (Aioi, et al., 2001). Skin barrier dysfunction has emerged as a critical driving force in the initiation and exacerbation of AD and as "driver" of disease activity (Cork, et al., 2009, Elias, et al., 2008), although it has once

Elias et al. proposed the outside-to-inside pathogenic mechanisms in AD for the following reasons: (1) the extent of the permeability barrier abnormality parallels the severity of the

animal model of AD particularly challenging (Scharschmidt &Segre, 2008).

been noted as a disease of immunological etiology (Leung &Bieber, 2003).

development of allergic responses (Jin, et al., 2009).

**1. Introduction** 
