XXXVIII Congreso de la Sociedad Española de Inmunología Clínica, Alergología y Asma Pediátrica
433
•
Primera línea:
defensa química:
AMPs
•
Segunda línea:
reconocimiento del
patógeno: TLR, que llevan a la
producción de IL-1 y activan
diferentes vías de señalización:
–
Citocinas inflamatorias
–
IF
–
Genes de linfocitos B y T,
estímulo
de la
tercera línea:
inmunidad adaptativa
Inmunidad innata
en la piel
¿Puede la Da favorecer la marcha atópica?
Hindawi Publishing Corporation
Journal of Allergy
Volume 2011, Article ID 279425, 5 pages
doi:10.1155/2011/279425
Review Article
Atopic Dermatitis and the Atopic March: What Is New?
Annalisa Patrizi,
1
Alessandro Pileri,
1
Federica Bellini,
2
Beatrice Raone,
1
Iria Neri,
1
and Giampaolo Ricci
2
1
Division of Dermatology, Department of Internal Medicine, Geriatrics and Nephrology, University of Bologna, Via Massarenti 1,
40138 Bologna, Italy
2
Department of Pediatrics, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy
Correspondence should be addressed to Annalisa Patrizi,
Received 8 April 2011; Accepted 14 June 2011
Academic Editor: Fabienne Ranc´e
Copyright © 2011 Annalisa Patrizi et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Objective
. In this paper the authors review the management of atopic dermatitis (AD) and the association between AD and allergic
respiratory diseases.
Data Sources
. PubMed databases, researching articles in the last 15 years.
Results
. Studies about atopic march
are cross-sectional population studies at di
ff
erent ages. They show that the most important predisposing factor for atopy is a
decrease of the filaggrin’s expression.
Conclusions
. The most modern theories seem to show that the most important factor which
starts the atopic march is represented by an impaired epidermal barrier. It causes an increase in skin permeability to allergens
that could induce sensitization even in the airways. The major predisposing factor is a primary inherited epithelial barrier defect
resulting from filaggrin gene mutation, but other factors may play a role in this complex mechanism. Further studies are needed
to focus on AD treatment and preventive strategies.
1. Introduction
Atopic dermatitis (AD) is the commonest chronic cutaneous
disease of childhood in the first years of life [1]. AD is often
the first manifestation of allergic diseases. Literature data
[2, 3] show a progression from AD to asthma: the so-called
atopic march
. In this paper we will focus reader’s attention
about the relationship between AD and respiratory allergic
diseases.
2. History of AD
AD has a long history. It was firstly described in 1892
by Besnier [4] who named it “prurigo diath´esique”. In
order to highlight a possible association between the skin
flare and genetic constitution, in 1927 Brocq suggested the
term “constitutional eczema”. Wise and Sulzberger in 1933
changed this name into “atopic dermatitis”, finally adopted
by Hanifin and Rajka in 1980 [5]. This is the current
denomination adopted in the USA, while in Europe the most
common definition is atopic eczema. In 2004 the World
Allergy Organisation (WAO) Committee suggested to call
“atopic eczema” any inflammatory condition determined
by an IgE reaction, suggesting that the presence of eczema
in atopic patients could be associated with or herald the
development of some allergic diseases such as rhinitis and
asthma [6].
3. Genetic State of Art
AD may be the first manifestation of allergic diseases and
may be the first step of the so-called
atopic march.
A crucial
role is played by filaggrin (filament-aggregating protein) that
is involved in the epidermal barrier function. It is important
for w ter permeability and for blocking the entry of microbes
and allergens [7]. Filaggrin aggregates the keratin filaments
and this process is essential for the formation of a normal
stratum corneum and for the hydration of the skin. The
filaggrin gene (FLG), located on chromosome 1q21 in
the epidermal di
ff
erentiation complex, encodes profilaggrin,
a phosphorylated protein, precursor of filaggrin protein.
Studie about FLG have underlined the link between early
childhood eczema and the subsequent development of
asthma. This is due to defective epidermal barrier function
