Article
Platelets Fuel the Inflammasome Activation of Innate Immune Cells
Registro en:
ROLFES, Verena et al. Platelets Fuel the Inflammasome Activation of Innate Immune Cells. Cell Reports, v. 31, n. 6, 107615, 2020
2211-1247
10.1016/j.celrep.2020.107615
Autor
Rolfes, Verena
Ribeiro, Lucas Secchim
Hawwari, Ibrahim
Böttcher, Lisa
Rosero, Nathalia
Maasewerd, Salie
Santos, Marina Lima Silva
Próchnicki, Tomasz
Silva, Camila Meirelles de Souza
Wanderley, Carlos Wagner de Souza
Rothe, Maximilian
Schmidt, Susanne V.
Stunden, H. James
Bertheloot, Damien
Rivas, Magali Noval
Fontes, Cor Jesus
Carvalho, Luzia Helena
Cunha, Fernando Queiroz
Latz, Eicke
Arditi, Moshe
Franklin, Bernardo Simoes
Resumen
The inflammasomes control the bioactivity of pro-inflammatory cytokines of the interleukin (IL)-1 family. The inflammasome assembled by NLRP3 has been predominantly studied in homogeneous cell populations in vitro, neglecting the influence of cellular interactions that occur in vivo. Here, we show that platelets boost the inflammasome capacity of human macrophages and neutrophils and are critical for IL-1 production by monocytes. Platelets license NLRP3 transcription, thereby enhancing ASC oligomerization, caspase-1 activity, and IL-1β secretion. Platelets influence IL-1β production in vivo, and blood platelet counts correlate with plasmatic IL-1β levels in malaria. Furthermore, we reveal an enriched platelet gene signature among the highest-expressed transcripts in IL-1β-driven autoinflammatory diseases. The platelet effect is independent of cell-to-cell contact, platelet-derived lipid mediators, purines, nucleic acids, and a host of platelet cytokines, and it involves the triggering of calcium-sensing receptors on macrophages. Hence, platelets provide an additional layer of regulation of inflammasomes and IL-1-driven inflammation. 2035-01-01