ROAMINPD

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

 Coordinatore 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

 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

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

cells    infection    dialysis    treatment    monocytic    peritoneal    broad    pd    models    tissue    macrophage    mouse    impact    immunity    monocytes    susceptibility    biology    homeostasis    monocyte    patients    functional   

 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.'

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