Skip to main content
Go to the home page of the European Commission (opens in new window)
English English
CORDIS - EU research results
CORDIS
Content archived on 2024-06-18

Hypercapnic Acidosis and NF-kB in Ventilator Induced Lung Injury: Developing strategies to minimize lung injury and facilitate repair

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.

Fields of science (EuroSciVoc)

CORDIS classifies projects with EuroSciVoc, a multilingual taxonomy of fields of science, through a semi-automatic process based on NLP techniques. See: https://op.europa.eu/en/web/eu-vocabularies/euroscivoc.

You need to log in or register to use this function

Keywords

Project’s keywords as indicated by the project coordinator. Not to be confused with the EuroSciVoc taxonomy (Fields of science)

Topic(s)

Calls for proposals are divided into topics. A topic defines a specific subject or area for which applicants can submit proposals. The description of a topic comprises its specific scope and the expected impact of the funded project.

Call for proposal

Procedure for inviting applicants to submit project proposals, with the aim of receiving EU funding.

ERC-2007-StG
See other projects for this call

Funding Scheme

Funding scheme (or “Type of Action”) inside a programme with common features. It specifies: the scope of what is funded; the reimbursement rate; specific evaluation criteria to qualify for funding; and the use of simplified forms of costs like lump sums.

ERC-SG - ERC Starting Grant

Host institution

UNIVERSITY OF GALWAY
EU contribution
€ 1 052 556,00
Address
UNIVERSITY ROAD
H91 Galway
Ireland

See on map

Region
Ireland Northern and Western West
Activity type
Higher or Secondary Education Establishments
Links
Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

No data

Beneficiaries (1)

My booklet 0 0