by Adrover, José M, Aroca-Crevillen, Alejandra, Crainiciuc, Georgiana, Ostos, Fernando, Rojas-Vega, Yeny, Rubio-Ponce, Andrea, Cilloniz, Catia, Bonzon-Kulichenko, Elena, Calvo, Enrique, Rico, Daniel, Moro, María A, Weber, Christian, Lizasoain, Ignacio, Torres, Antoni, Ruiz-Cabello, Jesus, Vázquez, Jesús and Hidalgo, Andrés
Abstract:
The antimicrobial functions of neutrophils are facilitated by a defensive armamentarium of proteins stored in granules, and by the formation of neutrophil extracellular traps (NETs). However, the toxic nature of these structures poses a threat to highly vascularized tissues, such as the lungs. Here, we identified a cell-intrinsic program that modified the neutrophil proteome in the circulation and caused the progressive loss of granule content and reduction of the NET-forming capacity. This program was driven by the receptor CXCR2 and by regulators of circadian cycles. As a consequence, lungs were protected from inflammatory injury at times of day or in mouse mutants in which granule content was low. Changes in the proteome, granule content and NET formation also occurred in human neutrophils, and correlated with the incidence and severity of respiratory distress in pneumonia patients. Our findings unveil a ‘disarming’ strategy of neutrophils that depletes protein stores to reduce the magnitude of inflammation.
Reference:
Programmed ‘disarming’ of the neutrophil proteome reduces the magnitude of inflammation. (Adrover, José M, Aroca-Crevillen, Alejandra, Crainiciuc, Georgiana, Ostos, Fernando, Rojas-Vega, Yeny, Rubio-Ponce, Andrea, Cilloniz, Catia, Bonzon-Kulichenko, Elena, Calvo, Enrique, Rico, Daniel, Moro, María A, Weber, Christian, Lizasoain, Ignacio, Torres, Antoni, Ruiz-Cabello, Jesus, Vázquez, Jesús and Hidalgo, Andrés), In Nature immunology, Nature Publishing Group, volume 273, 2020.
Bibtex Entry:
@article{Adrover:2020ih,
author = {Adrover, Jos{'e} M and Aroca-Crevillen, Alejandra and Crainiciuc, Georgiana and Ostos, Fernando and Rojas-Vega, Yeny and Rubio-Ponce, Andrea and Cilloniz, Catia and Bonzon-Kulichenko, Elena and Calvo, Enrique and Rico, Daniel and Moro, Mar{'i}a A and Weber, Christian and Lizasoain, Ignacio and Torres, Antoni and Ruiz-Cabello, Jesus and V{'a}zquez, Jes{'u}s and Hidalgo, Andr{'e}s},
title = {{Programmed 'disarming' of the neutrophil proteome reduces the magnitude of inflammation.}},
journal = {Nature immunology},
year = {2020},
volume = {273},
number = {2},
pages = {11--10},
month = jan,
publisher = {Nature Publishing Group},
affiliation = {Area of Cell and Developmental Biology, Fundaci{'o}n Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.},
doi = {10.1038/s41590-019-0571-2},
pmid = {31932813},
pmcid = {PMC7223223},
language = {English},
rating = {0},
date-added = {2020-01-19T17:52:34GMT},
date-modified = {2020-10-07T09:51:48GMT},
abstract = {The antimicrobial functions of neutrophils are facilitated by a defensive armamentarium of proteins stored in granules, and by the formation of neutrophil extracellular traps (NETs). However, the toxic nature of these structures poses a threat to highly vascularized tissues, such as the lungs. Here, we identified a cell-intrinsic program that modified the neutrophil proteome in the circulation and caused the progressive loss of granule content and reduction of the NET-forming capacity. This program was driven by the receptor CXCR2 and by regulators of circadian cycles. As a consequence, lungs were protected from inflammatory injury at times of day or in mouse mutants in which granule content was low. Changes in the proteome, granule content and NET formation also occurred in human neutrophils, and correlated with the incidence and severity of respiratory distress in pneumonia patients. Our findings unveil a 'disarming' strategy of neutrophils that depletes protein stores to reduce the magnitude of inflammation.},
url = {http://www.nature.com/articles/s41590-019-0571-2},
local-url = {file://localhost/Users/jruizcabello/Documents/JRC/biblio/Papers-folder/Library.papers3/Files/79/79C426FB-A175-40A6-9A6C-1D9EB4331EE4.pdf},
file = {{79C426FB-A175-40A6-9A6C-1D9EB4331EE4.pdf:/Users/jruizcabello/Documents/JRC/biblio/Papers-folder/Library.papers3/Files/79/79C426FB-A175-40A6-9A6C-1D9EB4331EE4.pdf:application/pdf;79C426FB-A175-40A6-9A6C-1D9EB4331EE4.pdf:/Users/jruizcabello/Documents/JRC/biblio/Papers-folder/Library.papers3/Files/79/79C426FB-A175-40A6-9A6C-1D9EB4331EE4.pdf:application/pdf}},
uri = {url{papers3://publication/doi/10.1038/s41590-019-0571-2}}
}