RELM-A IN THE LUNG

Expression and function or Resistin-like molecule alpha in asthma pathogenesis and fibrosis

Coordinatore	TEL AVIV UNIVERSITY    more  Organization address address: RAMAT AVIV city: TEL AVIV postcode: 69978 contact info Titolo: Ms. Nome: Lea Cognome: Pais Email: send email Telefono: 97236408774 Fax: 97236409697
Nazionalità Coordinatore	Israel [IL]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2009-RG
Funding Scheme	MC-IRG
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-07-01   -   2014-06-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	TEL AVIV UNIVERSITY  Organization address address: RAMAT AVIV city: TEL AVIV postcode: 69978 contact info Titolo: Ms. Nome: Lea Cognome: Pais Email: send email Telefono: 97236408774 Fax: 97236409697	IL (TEL AVIV)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Currently there is an epidemic of asthma in the western world and the incidence is rising in alarming rates. Experimentation in the asthma field has identified involvement of Th2 cytokines (e.g IL-4 and IL-13), chemokines, mucus hypersecretion, airway obstruction, eosinophilia, enhanced airway hyperreactivity to spasmogens in the asthmatic response and the presence of fibrosis. IL-4 and IL-13, “hallmark” Th2 associated cytokines are markedly elevated in the asthmatic lung and are central regulators of many of the hallmark features of disease and is now viewed as a critical cytokine in disease pathogenesis. Resistin is a hormone that was originally identified in adipose tissue and shown to promote insulin resistance and possibly obesity. However, it is now appreciated that resistin belongs to a newly defined family of resistin-like molecules (Relm) including Relm-alpha, Relm-beta and Relm-gamma that are potent innate immune regulators, and are implicated in Th2-associated immune responses. Indeed, Relm-alpha was originally identified in inflammatory zones associated with an experimental allergic airway disease model and has been called Found in Inflammatory Zones (FIZZ) 1. Recently, I have characterized a pro-inflammatory, regulatory role for Relm-alpha in experimental colitis. Furthermore, I have identified Relm-alpha as one of the highest upregulated IL-13 induced genes in the murine asthmatic lung. Collectively, implicating an important role for Relm-alpha in lung allergic inflammatory responses. The central hypothesis of this grant application is that allergen-induced lung inflammation and fibrosis are regulated by Relm-alpha. To define the role of Relm-alpha in such settings I aim to define the expression pattern, molecular regulation and cellular source for Relm-alpha expression following experimental-asthma and -fibrosis induction. Furthermore, I aim to define the function of Relm-alpha in experimental-asthma and -fibrosis. Finally, I will define the effects o'

Introduzione (Teaser)

Industrialised countries are experiencing a rise in asthma. Understanding the molecular events that culminate in disease pathophysiology is central for designing novel treatments.