IL-1β release by BMDM, from wild-type (<i>wt</i>) and <i>Nlrp3</i><sup>-/-</sup> mice, exposed to CoCrMo particles or Co<sup>2</sup><sup>+</sup>.

IL-1β release by BMDM, from wild-type (<i>wt</i>) and <i>Nlrp3</i><sup>-/-</sup> mice, exposed to CoCrMo particles or Co<sup>2</sup><sup>+</sup>.

<p>Bone marrow-derived macrophages (BMDM) were primed with 500 ng/mL of lipopolysaccharide for 3 h, then exposed to 3.4-μm spherical CoCrMo particles (<b>A</b>) or Co<sup>2+</sup> (<b>B</b>) for 18 h. Interleukin-1β (IL-1β) release was quantified by enzyme-l...

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Autor principal:	Nasteho Abdoulkader (22641176) (author)
Altres autors:	Jennifer Archibald (22641179) (author), Morgane Lignereux (22641182) (author), Eric A. Lehoux (2947641) (author), Isabelle Catelas (4909363) (author)
Publicat:	2025
Matèries:	Cell Biology Genetics Molecular Biology Neuroscience Biotechnology Immunology Developmental Biology Marine Biology Cancer Science Policy Infectious Diseases Virology reactive oxygen species process putatively linked 4 &# 956 >< sup >< 2 +</ sup ></ sup >), metal ions released div >< p 1 &# 946 3 +</ sup inflammatory response triggered determine whether il identifying mechanisms involved cathepsin b dependent 1β release induced nlrp3 inflammasome activation metal ions cathepsin b whereas activation inflammatory response >), nlrp3 whether nlrp3 nlrp3 inflammasome nlpr3 inflammasome wt </ whether caspase type (< therefore critical targeting nlrp3 occurred independently nlrp3 </ macrophage pro lysosomal destabilization induce il includes interleukin implant failure findings highlight dependent release deficient (< corrosion products casp1 </ bone marrow analysis suggested 1β release
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