The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Inflammasome-dependent IL-1β release depends upon membrane permeabilisation
Open accessAbstract
Interleukin-1β (IL-1β) is a critical regulator of the inflammatory response. IL-1β is not secreted through the conventional ER-Golgi route of protein secretion, and to date its mechanism of release has been unknown. Crucially, its secretion depends upon the processing of a precursor form following the activation of the multimolecular inflammasome complex. Using a novel and reversible pharmacological inhibitor of the IL-1β release process, in combination with biochemical, biophysical, and real-time single-cell confocal microscopy with macrophage cells expressing Venus-labelled IL-1β, we have discovered that the secretion of IL-1β after inflammasome activation requires membrane permeabilisation, and occurs in parallel with the death of the secreting cell. Thus, in macrophages the release of IL-1β in response to inflammasome activation appears to be a secretory process independent of nonspecific leakage of proteins during cell death. The mechanism of membrane permeabilisation leading to IL-1β release is distinct from the unconventional secretory mechanism employed by its structural homologues fibroblast growth factor 2 (FGF2) or IL-1α, a process that involves the formation of membrane pores but does not result in cell death. These discoveries reveal key processes at the initiation of an inflammatory response and deliver new insights into the mechanisms of protein release.
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Cites
Gout-associated uric acid crystals activate the NALP3 inflammasome
Martinon, F., Pétrilli, V., Mayor, A., Tardivel, A., & Tschopp, J. (2006) · Nature · doi:10.1038/nature04516 · Cited by 5,326
Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
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Molecular Physiology of P2X Receptors
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Activation and regulation of the inflammasomes
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The interleukin-1 family: back to the future
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“Interleukin-1β (IL-1β) is a proinflammatory cytokine that is central for host responses to infection.(1) IL-1β is produced as an inactive precursor called pro-IL-1β mainly by inflammatory cells of myeloid lineage.”
BackgroundUnderstanding the mechanism of IL-1β secretion
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Baroja-Mazo, A., Martín-Sánchez, F., Gomez, A. I., Martínez, C. M., Amores-Iniesta, J., Compan, V., Barberà-Cremades, M., Yagüe, J., Ruiz-Ortiz, E., Antón, J., et al. (2014) · Nature Immunology · doi:10.1038/ni.2919 · Cited by 790 · cited 1×
“Caspase-1 activity is suggested as the main driver of a specific programme of cell death termed pyroptosis that is associated with the leakage of intracellular proteins, including the release of large inflammasome complexes.(33,34) Our data show that both mechanisms, membrane permeability and caspase-1 activity, are i…”
BackgroundQu, Y., Franchi, L., Nunez, G., & Dubyak, G. R. (2007) · The Journal of Immunology · doi:10.4049/jimmunol.179.3.1913 · Cited by 563
Caspase-1-dependent processing of pro-interleukin-1β is cytosolic and precedes cell death
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Self-citationP2X7 receptor‐stimulation causes fever via PGE2 and IL‐1β release
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Cited by
The gasdermins, a protein family executing cell death and inflammation
Broz, P., Pelegrín, P., & Shao, F. (2020) · Nature Reviews Immunology · doi:10.1038/s41577-019-0228-2 · Cited by 1,641
Self-citationGasdermins: Effectors of Pyroptosis
Kovacs, S. B., & Miao, E. A. (2017) · Trends in Cell Biology · doi:10.1016/j.tcb.2017.05.005 · Cited by 1,379
Role of pyroptosis in inflammation and cancer
Wei, X., Xie, F., Zhou, X., Wu, Y., Yan, H., Liu, T., Huang, J., Wang, F., Zhou, F., & Zhang, L. (2022) · Cellular & Molecular Immunology · doi:10.1038/s41423-022-00905-x · Cited by 699
Pharmacological Inhibitors of the NLRP3 Inflammasome
Zahid, A., Li, B., Kombe, A. J. K., Jin, T., & Tao, J. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02538 · Cited by 671
Noncanonical inflammasome signaling elicits gasdermin D–dependent neutrophil extracellular traps
Chen, K. W., Monteleone, M., Boucher, D., Sollberger, G., Ramnath, D., Condon, N. D., von Pein, J. B., Broz, P., Sweet, M. J., & Schroder, K. (2018) · Science Immunology · doi:10.1126/sciimmunol.aar6676 · Cited by 639
Metadata
- Authors
- Martín-Sánchez, F., Diamond, C., Zeitler, M., Gomez, A. I., Baroja-Mazo, A., Bagnall, J., Spiller, D., White, M., Daniels, M. J. D., Mortellaro, A., Peñalver, M., Paszek, P., Steringer, J. P., Nickel, W., Brough, D., & Pelegrín, P.
- Venue
- Cell Death & Differentiation
- Published
- 2016-02-12
- Volume
- 23
- Issue
- 7
- Pages
- 1219-1231
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W2269721101
- Cited by
- 279
- References
- 10
- FWCI
- 11.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Martín-Sánchez, F., Diamond, C., Zeitler, M., Gomez, A. I., Baroja-Mazo, A., Bagnall, J., Spiller, D., White, M., Daniels, M. J. D., Mortellaro, A., Peñalver, M., Paszek, P., Steringer, J. P., Nickel, W., Brough, D., & Pelegrín, P. (2016). Inflammasome-dependent IL-1β release depends upon membrane permeabilisation. Cell Death & Differentiation. https://doi.org/10.1038/cdd.2015.176
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