RT Journal Article
T1 SP-D attenuates LPS-induced formation of human neutrophil extracellular traps (NETs), protecting pulmonary surfactant inactivation by NETs
A1 Arroyo, Raquel
A1 Khan, MerajAlam
A1 Echaide Torreguitar, Mercedes
A1 Pérez-Gil, Jesús
A1 Palaniyar, Nades
AB An exacerbated amount of neutrophil extracellular traps (NETs) can cause dysfunction of systems during inflammation. However, host proteins and factors that suppress NET formation (NETosis) are not clearly identified. Here we show that an innate immune collectin, pulmonary surfactant protein-D (SP-D), attenuates lipopolysaccharide (LPS)-mediated NETosis in human neutrophils by binding to LPS. SP-D deficiency in mice (Sftpd−/−) leads to excess NET formation in the lungs during LPS-mediated inflammation. In the absence of SP-D, NETs inhibit the surface-active properties of lung surfactant, essential to prevent the collapse of alveoli, the air breathing structures of the lungs. SP-D reverses NET-mediated inhibition of surfactant and restores the biophysical properties of surfactant. To the best of our knowledge, this study establishes for the first time that (i) SP-D suppresses LPS-mediated NETosis, (ii) NETs inhibit pulmonary surfactant function in the absence of SP-D, and (iii) SP-D can restore NET-mediated inhibition of the surfactant system.
PB Nature Research
SN 2399-3642
YR 2019
FD 2019-12-16
LK https://hdl.handle.net/20.500.14352/6544
UL https://hdl.handle.net/20.500.14352/6544
LA eng
NO Ministerio de Ciencia, Innovación y Universidades (MICINN)
NO Comunidad de Madrid/FEDER
NO Cystic Fibrosis Canada discovery grant
NO Natural Sciences and Engineering Research Council of Canada
DS Docta Complutense
RD 27 nov 2025