Page 24 - MemoriaES-Eng

RESEARCH PROGRAMMES

1. To identify genes/processes that are deregulated in preclinical models of
Aims and
ALI (assessed by functional genomics), or that constitute hits in genome-
objectives
wide association studies being conducted. To examine whether genetic variants

of those genes are associated with acute lung injury (ALI) and the acute respiratory
distress syndrome (ARDS) development and outcome (mortality or protection). To

find new enigmatic genes that can explain the diversity of clinical presentation of

ALI/ARDS, the response to current medical treatment, and the individual’s genetic
predisposition.

2. To discover biomarkers of ALI among the three most relevant families of mark-

ers (i.e., inflammation-cytokine, endothelial related and epithelial derived markers).

Determine the utility of MRS and MS as biomarkers of ALI. To validate volatile organ-
ic compounds in airway fluid and exhaled breath samples collected by non-invasive

or minimally invasive as biomarkers of ALI/ARDS. To determine specific biomarkers

for the early detection of alterations in CNS function in ALI/ARDS at the local brain
level (alterations in tissue architecture, and mapping of biological markers related to

neuronal activation of early genes, apoptosis and inflammation); and to define their
correlation with systemic biomarkers.

3. To demonstrate a key role of TLR/NLR receptor activation in the pathogen-
esis of ALI. These effects will be studied in animal models of ALI and in serum from

patients with ALI, as well as in different cell types and in isolated ventilated perfused

lung model.

4. To define the relationship of asynchronies to clinically relevant outcomes
in patients with ALI, in order to define therapeutic targets based on ventilatory

management and to define ventilatory management strategies

5. To explore lung repair mechanisms that are initiated immediately follow-

ing the insult leading to ALI/ARDS (i.e. sepsis, VILI). To study interactions between
initiating factors, structural pulmonary elements, and signalling pathways that are

involved in lung repair.

To define biochemical factors determining changes in surfactant function and struc-

ture in a rat model of ALI. To define mechanisms of alveolar repair, by means of stem
cells, in decellularized lung scaffolds and in a lung-on-a-chip model. To use of adult

stem cells in treatment.

6. To spread knowledge and evidence providing new insights and training on

acute lung injury mechanisms and lung repair.

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