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• L4. Molecular interactions between alveolar protein SP-A and nanoparticles (CRP

on New Therapies to Treat Respiratory Diseases).

• L5. The high-stretch ventilation impact in the alveolar space and in particular

on the composition, structure, and functional activity of lung surfactant (CRP on
Acute Lung Injury).

• L6. Benefits of intratracheal treatment of natural and synthetic surfactants as

well as anti-inflammatory agents in acute lung injury induced by mechanical
ventilation (CRP on Acute Lung Injury).

This research has direct relevance for the development of new therapies for in-
flammatory and infectious lung diseases.

• M V, l-S A, Z F, u P, S A, c c .. Prophylaxis
onForteóPeZáncHeZurBAnoSSettioléASAlSet AlMost relevant ñ
with nebulized liposomal amphotericin B for Aspergillus infection in lung transplant
scientific patients does not cause changes in the lipid content of pulmonary surfactant.J Heart

articles
Lung Transplant. 2013 Mar;32(3):313-9.

• cAAdAS o, cASAlS c. Differential scanning calorimetry of protein-lipid interactions.
Methods Mol Biol. 2013;974:55-71.

RELEVANT RESEARCH PROJECT: SAF2012-32728 (2013-2015) Lung surfactant as
Highlights
protector and modulator of lung infection and inflammation. Funded by Spanish Mi-

nistry of Economy and Competitiveness. Principal Investigator: Cristina Casals.

RELEVANT RESULTS:
• Line 1: We demonstrated that internalized lung surfactant vesicles containing

human surfactant protein C affect the state of macrophage activation induced by

bacterial lipopolysaccharide and inhibit expression of inflammatory mediators by
human pneumocytes induced by respiratory syncytial virus.

• Line 2: We demonstrated that SP-A and SP-BN acted synergistically to kill capsulated

K. pneumoniae (serotype K2) at neutral pH, where neither of these proteins had
bactericidal activity. In addition, we found that i.t. administration of SP-A and SP-

BNconfersprotectionagainstK.pneumoniaeK2infection.Moreover, SP-A/SP-BN

administration 6 or 24 h after pathogen inoculation (once K. pneumoniae infection
was established) resulted in a 4-fold decrease of lung bacterial burden, thereby

indicating its therapeutic effect.

• Line 5: We demonstrated that ventilator-induced lung injury (VILI) only occurred
in animal models when surfactant was inactivated. There was a direct link between

a pronounced proinflammatory response and surfactant inactivation. In addition,
we showed that an attenuate inflammatory response together with increasing

secretion of endogenous, fully active, surfactant, protected the lung against the 13
20
hypoxia and the protein leakage.
T
OR
DOCTORAL THESIS: 14/10/2014- Virginai Egido. “Lung response against ventilator P
induced lung injury: role of pulmonary surfactant”. Complutense University of Ma- RE
L
drid. Doctoral Program: Biochemistry, Molecular Biology and Biomedicine (“Mention A
towards Excellence” by the Ministry of Science and Education). Evaluation: Excellent NU
N
“cum laude” Director: Dr. Cristina Casals.
A
S /
INTERNATIONAL COLLABORATION: 1) Prof. Dr. Timothy Weaver, Cincinatti Children’s E
Hospital (Ohio, USA), supervisor of Juan Manuel Coya during his predoctoral stay in ER
B
USA-2013, granted by the Spanish Personnel Research Training Program; 2) Prof. Dr. CI

Jan Johansson, Karolinska Institute, Stockholm Sweden (European Research Project
submission in 2013 and 2014); 3) Collaboration agreement with Nycomed GmbH- 95

Takeda in the biomed/biotech field.