HA-NFKB-VILI
Hypercapnic Acidosis and NF-kB in Ventilator Induced Lung Injury: Developing strategies to minimize lung injury and facilitate repair
| Coordinatore | NATIONAL UNIVERSITY OF IRELAND, GALWAY
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| Nazionalità Coordinatore | Ireland [IE] |
| Totale costo | 1˙052˙556 € |
| EC contributo | 1˙052˙556 € |
| Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | ERC-2007-StG |
| Funding Scheme | ERC-SG |
| Anno di inizio | 2009 |
| Periodo (anno-mese-giorno) | 2009-01-01 - 2013-12-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
NATIONAL UNIVERSITY OF IRELAND, GALWAY
Organization address
address: University Road - contact info |
IE (GALWAY) | hostInstitution | 0.00 |
| 2 |
NATIONAL UNIVERSITY OF IRELAND, GALWAY
Organization address
address: University Road - contact info |
IE (GALWAY) | hostInstitution | 0.00 |
Mappa
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Obiettivo del progetto (Objective)
'Acute Respiratory Distress Syndrome and Acute Lung Injury [ALI/ARDS] are devastating diseases, causing over 20,000 deaths annually in the US. Mechanical ventilation may worsen ALI/ARDS, a process termed Ventilator Induced Lung Injury [VILI]. Hypercapnic acidosis (HA) is a central component of lung ventilatory strategies to minimize VILI, and is a potent biologic agent, exerting a myriad of effects on diverse biologic pathways. Deliberately induced HA is protective in multiple lung injury models. However, HA may inhibit the host response to bacterial sepsis. Furthermore, HA may retard the repair process and slow recovery following ALI/ARDS. Hence, the diverse biologic actions of HA may result in net beneficial – or deleterious – effects depending on the specific context. An alternative approach is to manipulate a single key effector pathway, central to the protective effects of HA, which would also be effective in patients in whom hypercapnia is contra-indicated. Hypercapnia attenuates NF-kB activation, and may exert its effects – both beneficial and deleterious – via this mechanism. NF-kB is a pivotal regulator of the pro-inflammatory response, but is also a key epithelial cytoprotectant. Selective modulation of the NF-kB pathway, at the pulmonary epithelial surface, may accentuate the beneficial effects of HA on injury but minimize the potential for delayed tissue repair. We will investigate the contribution of NF-kB to the effects of HA, and characterize the direct effects modulation of NF-kB, in both in vitro and preclinical models of lung injury and repair. We will utilize pulmonary gene therapy, which facilitates delivery of high quantities of the therapeutic agent directly to the injury site, to maximize the potential for therapeutic benefit. These studies will provide novel insights into: key pathways contributing to lung injury and to repair; the role of HA and NF-kB in these processes; and the potential of pulmonary gene therapy in ALI/ARDS.'