Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 285, Issue 30, Pages 23145-23156Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M109.072793
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Funding
- British Heart Foundation [FS/06/004, FS/05/081/19423]
- Medical Research Council [G116/170]
- Research Councils UK
- Novartis
- National Institute of Health Research
- MRC [G116/170] Funding Source: UKRI
- Medical Research Council [G116/170] Funding Source: researchfish
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The processing and regulated secretion of IL-1 beta are critical points of control of the biological activity of this important pro-inflammatory cytokine. IL-1 beta is produced by both monocytes and macrophages, but the rate and mechanism of release differ according to the differentiation status and the origin of these cells. We aimed to study the control of processing and release in human blood monocytes and human monocyte-derived macrophages. Toll-like receptor (TLR)-induced IL-1 beta production and release were investigated for dependence upon caspase-1, P2X7 receptor activation, and loss of membrane asymmetry associated with microvesicle shedding. TLR agonists induced P2X7 receptor-dependent IL-1 beta release in both monocytes and macrophages; however, only monocytes also showed P2X7 receptor-independent release of mature IL-1 beta. Furthermore, in monocytes ATP-mediated PS exposure could be activated independently of IL-1 beta production. Release of IL-1 beta from monocytes showed selectivity for specific TLR agonists and was accelerated by P2X7 receptor activation. Human monocytes released more IL-1 beta/cell than macrophages. These data have important implications for inflammatory diseases that involve monocyte activation and IL-1 release.
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