Programmed ‘disarming’ of the neutrophil proteome reduces the magnitude of inflammation

Jose M. Adrover, Alejandra Aroca-Crevillén, Georgiana Crainiciuc, Fernando Ostos, Yeny Rojas-Vega, Andrea Rubio-Ponce, Catia Cilloniz, Elena Bonzón-Kulichenko, Enrique Calvo, Daniel Rico, María A. Moro, Christian Weber, Ignacio Lizasoaín, Antoni Torres, Jesús Ruiz-Cabello, Jesús Vázquez, Andrés Hidalgo

Producción científica: Artículo CientíficoArtículo originalrevisión exhaustiva

172 Citas (Scopus)


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.

Idioma originalInglés estadounidense
Páginas (desde-hasta)135-144
PublicaciónNature Immunology
EstadoIndizado - 1 feb. 2020
Publicado de forma externa

Nota bibliográfica

Publisher Copyright:
© 2020, The Author(s), under exclusive licence to Springer Nature America, Inc.


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