EMBARGOED FOR RELEASE
Wednesday, 7 December 2011
Sofia Dorsano, email@example.com
Note to media: See abstract 4172
Blocking of keratinocytic TSLP may limit epicutaneous sensitization
and prevent atopic march
CANCÚN – Juan Manuel Leyva Castillo, and colleagues from Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC, Strasbourg, France), today presented their work on the role of the skin in the initiation of the development of allergic respiratory symptoms.
Atopic dermatitis (AD or eczema) often precedes the development of asthma and allergic rhinitis in atopic subjects, a phenomenon known as the atopic march. An important role of epicutaneous sensitization has been recognized in this context, the factors involved remain poorly understood. Previous studies by the same investigators using mouse models have shown that induced over-expression of thymic stromal lymphopoietin (TSLP) in the superficial skin cells called keratinocytes not only triggers AD but also aggravates experimental asthma induced by systemic sensitization and airway challenge by ovalbumin (OVA) suggesting that TSLP represents an important factor linking AD to asthma.
The current study revealed that keratinocyte TSLP depleted mice develop a less severe airway allergic inflammation and a reduced airway hyperresponsiveness after epicutaneous sensitization. In contrast, overproduction of keratinocytic TSLP boosts the epicutaneous sensitization and triggers an aggravated asthma.
According to Professor Yehia El-Gamal, of the Children’s Hospital, Ain Shams University in Cairo, Egypt, “This shows an important role for keratinocytic TSLP in developing epicutaneous sensitization, generating allergic skin inflammation, and triggering the atopic march. Thus, blocking the expression or activity of keratinocytic TSLP might be helpful to limit epicutaneous sensitization and prevent the atopic march.”
This study is supported by CNRS, INSERM, ARI and ANR projects (07-PHYSIO-002–01 and JCJC-1106-01).
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