ASC and NLRP3 impair host defense during lethal pneumonia caused by serotype 3 Streptococcus pneumoniae in mice.
van Lieshout, Miriam H P; de Vos, Alex F; Dessing, Mark C; de Porto, Alexander P N A; de Boer, Onno J; de Beer, Regina; Terpstra, Sanne; Florquin, Sandrine; Van't Veer, Cornelis; van der Poll, Tom.
Eur J Immunol
; 48(1): 66-79, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28971472
The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response.
Phosphorylation of the adaptor ASC acts as a molecular switch that controls the formation of speck-like aggregates and inflammasome activity.
NLRP3 activation and mitosis are mutually exclusive events coordinated by NEK7, a new inflammasome component.
NLRP3 and ASC differentially affect the lung transcriptome during pneumococcal pneumonia.
The adaptor ASC has extracellular and 'prionoid' activities that propagate inflammation.
Inflammasome-dependent Mechanisms Involved in Sensing and Restriction of Bacterial Replication.
The PYHIN Protein p205 Regulates the Inflammasome by Controlling Asc Expression.
An additional piece in the puzzle of neutrophil-derived IL-1ß: the NLRP3 inflammasome.
The NLRP3 inflammasome is active but not essential in endotoxin-induced uveitis.