ROAMINPD

The role of altered monocyte activity in the long-term potential of peritoneal dialysis as a therapy

Coordinatore	CARDIFF UNIVERSITY    more  Organization address address: Newport Road 30-36 city: CARDIFF postcode: CF24 ODE contact info Titolo: Ms. Nome: Eevi Cognome: Laukkanen Email: send email Telefono: +44 29 20870114 Fax: +44 29 20874189
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	210˙092 €
EC contributo	210˙092 €
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-2010-IIF
Funding Scheme	MC-IIF
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-08-01   -   2013-07-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	CARDIFF UNIVERSITY  Organization address address: Newport Road 30-36 city: CARDIFF postcode: CF24 ODE contact info Titolo: Ms. Nome: Eevi Cognome: Laukkanen Email: send email Telefono: +44 29 20870114 Fax: +44 29 20874189	UK (CARDIFF)	coordinator	210˙092.80

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 Obiettivo del progetto (Objective)

'Recurrent infection remains the major reason for treatment failure in patients treated for renal failure with peritoneal dialysis (PD). The underlying hypothesis of this study is that modification of peritoneal monocyte/macrophage biology by PD alters tissue homeostasis, susceptibility to infection and the development of immunity to re-infection, compromising the long-term potential of peritoneal dialysis as a therapy. In spite of their role in peritoneal host defence and tissue homeostasis, the immunobiology of peritoneal macrophages remains poorly understood. Peritoneal monocytic cells derived from PD patients are depleted throughout the course of PD and exhibit increasing signs of immaturity with reduced capacity to respond to LPS compared to peripheral blood monocytes and a propensity to spontaneous activation in vitro. It has been suggested that these cells are polarised in their immune responsiveness towards an anti-inflammatory phenotype. Our broad experience of mouse models has highlighted extensive macrophage heterogeneity and has established a broad gene expression database. We aim to: 1. complete the first systematic and detailed study of the impact of peritoneal dialysis on the monocyte/macrophage system, including the identification of corresponding cellular subsets between mouse models and human. 2. assess the impact of this altered cell biology on functional responses of PD monocytic cells to infectious challenge, the regulation of immunity and tissue damage. Our combined experience and novel datasets mean that we will develop a detailed understanding of the functional alterations in the monocyte/macrophage-lineage and the impacts these have on susceptibility to infection and treatment failure. A better mechanistic characterisation of changes in peritoneal monocytes may translate into novel therapeutic interventions that will have direct application for improving outcomes in PD patients and the potential for long-term PD treatment.'