AI Article Synopsis
- The NLRP3 inflammasome plays a key role in inflammation by activating caspase-1, which helps process and release the cytokine IL-1β, important in various diseases.
- Researchers discovered that when caspase-1 is activated, NLRP3 inflammasome particles are released from macrophages, which can further stimulate inflammation.
- Oligomeric ASC protein particles were found in the serum of patients with certain inflammatory conditions, indicating that the NLRP3 inflammasome can enhance inflammatory responses beyond the cell it originates from.
Article Abstract
Assembly of the NLRP3 inflammasome activates caspase-1 and mediates the processing and release of the leaderless cytokine IL-1β and thereby serves a central role in the inflammatory response and in diverse human diseases. Here we found that upon activation of caspase-1, oligomeric NLRP3 inflammasome particles were released from macrophages. Recombinant oligomeric protein particles composed of the adaptor ASC or the p.D303N mutant form of NLRP3 associated with cryopyrin-associated periodic syndromes (CAPS) stimulated further activation of caspase-1 extracellularly, as well as intracellularly after phagocytosis by surrounding macrophages. We found oligomeric ASC particles in the serum of patients with active CAPS but not in that of patients with other inherited autoinflammatory diseases. Our findings support a model whereby the NLRP3 inflammasome, acting as an extracellular oligomeric complex, amplifies the inflammatory response.
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| http://dx.doi.org/10.1038/ni.2919 | DOI Listing |
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