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The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response
Open accessAbstract
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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“They can also be recognized by neighboring microglia as a danger signal and induce inflammatory responses including activation of the NLRP3 inflammasome, thereby propagating inflammation [70–72].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [71]
In the citing paper
“In turn, NLRP3 inflammasome activity leads to the extracellular release of ASC particles that may function as danger signals (246).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [246]
In the citing paper
“Increased expression and activity of the NLRP3 inflammasome machinery in circulating immune cells of patients affected by depression (245), bipolar disorder (246), and ASD (226), have been reported.”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [246]
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Inflammasome‐associated cell death: Pyroptosis, apoptosis, and physiological implications
Tsuchiya, K. (2020) · Microbiology and Immunology · doi:10.1111/1348-0421.12771 · Cited by 245
“Extracellular ASC specks may be taken up by phagocytes, in which the aggregates may activate caspase‐1 to sustain and spread inflammation, indicating a role for calpains in the propagation of inflammasome responses.(45) By contrast, the influx of Ca due to plasma membrane damage also activates membrane repair programs…”
BackgroundThe NLRP3 and Pyrin Inflammasomes: Implications in the Pathophysiology of Autoinflammatory Diseases
de Torre‐Minguela, C., Mesa-del-Castillo, P., & Pelegrín, P. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00043 · Cited by 251
“Mutant NLRP3 drives a constitutive hyperactivity of inflammasome, activation of caspase-1, and an excessive unregulated release of IL-1β, although systemic circulating levels of IL-1β during inflammatory flares are in most cases undetectable (11, 147).”
BackgroundTargeting Neuroinflammation to Treat Alzheimer’s Disease
Ardura-Fabregat, A., Boddeke, E., Boza‐Serrano, A., Brioschi, S., Castro‐Gomez, S., Ceyzériat, K., Dansokho, C., Dierkes, T., Gelders, G., Heneka, M. T., et al. (2017) · CNS Drugs · doi:10.1007/s40263-017-0483-3 · Cited by 241
Martínez-García, J. J., Martínez-Banaclocha, H., Angosto-Bazarra, D., de Torre-Minguela, C., Baroja-Mazo, A., Alarcón-Vila, C., Martínez-Alarcón, L., Amores-Iniesta, J., Martín-Sánchez, F., Ercole, G. A., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-10626-x · Cited by 233
Targeting Microglial α-Synuclein/TLRs/NF-kappaB/NLRP3 Inflammasome Axis in Parkinson’s Disease
Li, Y., Xia, Y., Yin, S., Wan, F., Hu, J., Kou, L., Sun, Y., Wu, J., Zhou, Q., Huang, J., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.719807 · Cited by 230
Caspase-8 as an Effector and Regulator of NLRP3 Inflammasome Signaling
Antonopoulos, C. H., Russo, H. M., Sanadi, C. E. E., Martin, B. N., Li, X., Kaiser, W. J., Mocarski, E. S., & Dubyak, G. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.652321 · Cited by 232
“An alternative mechanism for the delayed propidium2 uptake in Casp1/11 / DC AUGUST 14, 2015 • VOLUME 290 • NUMBER 33 JOURNAL OF BIOLOGICAL CHEMISTRY 20181 may involve a canonical caspase-8-driven apoptotic cascade that facilitates caspase-3-mediated proteolytic gating of pannexin-1 channels that are also expressed in…”
BackgroundInfluentialThe NLRP3 inflammasome is activated by nanoparticles through ATP, ADP and adenosine
Baron, L., Gombault, A., Fanny, M., Villeret, B., Savigny, F., Guillou, N., Panek, C., Bert, M. L., Lagente, V., Rassendren, F., et al. (2015) · Cell Death and Disease · doi:10.1038/cddis.2014.576 · Cited by 221
Structural mechanisms of inflammasome assembly
Lu, A. Z., & Wu, H. (2014) · FEBS Journal · doi:10.1111/febs.13133 · Cited by 231
Beclin1‐driven autophagy modulates the inflammatory response of microglia via NLRP3
Houtman, J., Freitag, K., Gimber, N., Schmoranzer, J., Heppner, F. L., & Jendrach, M. (2019) · The EMBO Journal · doi:10.15252/embj.201899430 · Cited by 213
Microglial PGC-1α protects against ischemic brain injury by suppressing neuroinflammation
Han, B., Jiang, W., Cui, P., Zheng, K., Dang, C., Wang, J., Li, H., Chen, L., Zhang, R., Wang, Q. M., et al. (2021) · Genome Medicine · doi:10.1186/s13073-021-00863-5 · Cited by 211
“Previous studies have suggested that the NLRP3 inflammasome plays a crucial role in amplifying the inflammatory response [28].”
BackgroundCathepsin B Is Required for NLRP3 Inflammasome Activation in Macrophages, Through NLRP3 Interaction
Chevriaux, A., Pilot, T., Dérangère, V., Simonin, H., Martine, P., Chalmin, F., Ghiringhelli, F., & Rébé, C. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.00167 · Cited by 202
“Once constituted, the NLRP3 inflammasome is then secreted in cell supernantant and can amplify the inflammatory response by activating inflammasomes and caspase-1 in neighboring cells (Baroja-Mazo et al., 2014; Franklin et al., 2014).”
BackgroundBiological and clinical roles of IL-18 in inflammatory diseases
Landy, E., Carol, H. A., Ring, A. M., & Canna, S. (2023) · Nature Reviews Rheumatology · doi:10.1038/s41584-023-01053-w · Cited by 218
“macrophages 38,39 .”
Systemic autoinflammatory diseases
Krainer, J., Siebenhandl, S., & Weinhäusel, A. (2020) · Journal of Autoimmunity · doi:10.1016/j.jaut.2020.102421 · Cited by 194
The role of IL-1B in breast cancer bone metastasis
Tulotta, C., & Ottewell, P. D. (2018) · Endocrine Related Cancer · doi:10.1530/erc-17-0309 · Cited by 192
Chloride regulates dynamic NLRP3-dependent ASC oligomerization and inflammasome priming
Green, J., Yu, S., Martín‐Sánchez, F., Pelegrín, P., López‐Castejón, G., Lawrence, C. B., & Brough, D. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1812744115 · Cited by 200
“The inflammasome specks released from pyroptotic cells can also further contribute to inflammatory responses (10, 11).”
BackgroundResponse of host inflammasomes to viral infection
Chen, I.-Y., & Ichinohe, T. (2014) · Trends in Microbiology · doi:10.1016/j.tim.2014.09.007 · Cited by 198
β-amyloid, microglia, and the inflammasome in Alzheimer’s disease
Gold, M., & El Khoury, J. (2015) · Seminars in Immunopathology · doi:10.1007/s00281-015-0518-0 · Cited by 187
Molecular mechanisms of inflammasome signaling
Mathur, A., Hayward, J. A., & Man, S. M. (2017) · Journal of Leukocyte Biology · doi:10.1189/jlb.3mr0617-250r · Cited by 192
Inflammatory outcomes of apoptosis, necrosis and necroptosis
Davidovich, P. B., Kearney, C. J., & Martin, S. J. (2014) · Biological Chemistry · doi:10.1515/hsz-2014-0164 · Cited by 190
“5 / 21 addition to mature IL-1β, whole inflammasome particles are released in response to agents that promote maturation of this cytokine (Baroja-Mazo et al., 2014; Franklin et al., 2014), which is consistent with the interpretation that cell death is a primary driver of IL-1β release.”
BackgroundMünzer, P., Negro, R., Fukui, S., Meglio, L. D., Aymonnier, K., Chu, L., Cherpokova, D., Gutch, S., Sorvillo, N., Shi, L. S., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.683803 · Cited by 197
“Indeed, ASC has been described as a “prionoid”, that, when phagocytosed by macrophages, induce inflammasome assembly (27, 71, 72).”
BackgroundGomez‐Lopez, N., Galaz, J., Miller, D., Farías, M., Liu, Z., Arenas‐Hernandez, M., Garcia‐Flores, V., Shaffer, Z., Greenberg, J. M., Theis, K. R., et al. (2022) · Reproduction · doi:10.1530/rep-22-0046 · Cited by 194
Integrated NLRP3, AIM2, NLRC4, Pyrin inflammasome activation and assembly drive PANoptosis
Oh, S., Lee, J., Oh, J.-E., Yu, G., Ryu, H., Kim, D., & Lee, S. (2023) · Cellular and Molecular Immunology · doi:10.1038/s41423-023-01107-9 · Cited by 192
Choulaki, C., Papadaki, G., Repa, A., Kampouraki, E., Kambas, K., Ritis, K., Bertsias, G. K., Boumpas, D. T., & Sidiropoulos, P. I. (2015) · Arthritis Research & Therapy · doi:10.1186/s13075-015-0775-2 · Cited by 187
“Recently, it has been shown that in mouse bone-marrowderived macrophages (BMDMs), the activation of inflammasomes resulted in the extracellular release of active inflammasome oligomers as particles that acted extracellularly as danger signals to amplify the inflammatory response by activating caspase-1 [45].”
BackgroundPost-ischemic inflammation regulates neural damage and protection
Shichita, T., Ito, M., & Yoshimura, A. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00319 · Cited by 188
Poh, L., Kang, S.-W., Baik, S., Ng, G. Y. Q., She, D. T., Balaganapathy, P., Dheen, S. T., Magnus, T. U., Gelderblom, M., Sobey, C. G., et al. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.09.001 · Cited by 190
Nanobodies that block gating of the P2X7 ion channel ameliorate inflammation
Danquah, W., Meyer‐Schwesinger, C., Rissiek, B., Pinto, C., Prat, A. S., Amadi, M., Iacenda, D., Knop, J., Hammel, A., Bergmann, P., et al. (2016) · Science Translational Medicine · doi:10.1126/scitranslmed.aaf8463 · Cited by 191
Ferulic acid inhibits neuro-inflammation in mice exposed to chronic unpredictable mild stress
Liu, Y., Shen, J.-D., Xu, L., Li, H., Li, Y., & Yi, L. (2017) · International Immunopharmacology · doi:10.1016/j.intimp.2017.02.007 · Cited by 185
“NLRP3 inflammasome, the best characterized inflammasome, mediates the processing and release of the leaderless cytokine IL-1β and thereby amplifies the inflammatory response [35].”
BackgroundAmores, J., Barberà-Cremades, M., Martínez, C. M., Pons, J. A., Revilla‐Nuin, B., Martínez-Alarcón, L., Virgilio, F. D., Parrilla, P., Baroja‐Mazo, A., & Pelegrín, P. (2017) · Cell Reports · doi:10.1016/j.celrep.2017.11.079 · Cited by 187
“BMDM were obtained from wild-type or P2rx7-/- mice using 25% of L-cell conditioned media as previously described (Baroja-Mazo et al., 2014). pmeLuc cells were maintained in DMEM:F12 (1:1) supplemented with 10% foetal calf serum (FCS), 2mM glutamax 1% and G418 0.2 mg/ml (Acros Organic).”
MethodInfluential
Metadata
- Authors
- 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., Buján, S., Couillin, I., Brough, D., Arostegui, J. I., & Pelegrín, P.
- Affiliations
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (ES)
- University of Manchester (GB)
- Hospital Clínic de Barcelona (ES)
- Hospital Sant Joan de Déu Barcelona (ES)
- Vall d'Hebron Hospital Universitari (ES)
- Université d'Orléans (FR)
- ORCID
- Venue
- Nature Immunology
- Published
- 2014-06-22
- Volume
- 15
- Issue
- 8
- Pages
- 738-748
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2143119237
- Cited by
- 790
- References
- 50
- Citations by year
- 2026: 28 · 2025: 39 · 2024: 41 · 2023: 63 · 2022: 81 · 2021: 84 · 2020: 86 · 2019: 68 · 2018: 74 · 2017: 88 · 2016: 60 · 2015: 57 · 2014: 20
- FWCI
- 30.77
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Hispana (publishedVersion, cc-by-nc-nd)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Hematology › Autoimmune and Inflammatory Disorders Research
- Keywords
- NLRP3 inflammasome, caspase-1, IL-1β processing, cryopyrin-associated periodic syndromes, macrophages, autoinflammatory disease, phagocytosis
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Cells, Cultured, Cytoskeletal Proteins, Humans, Inflammation, Macrophages, Mice, Inbred C57BL, Phagocytosis, Signal Transduction, Mice, Knockout, Caspases, Caspase 1, Apoptosis Regulatory Proteins, Mice, CARD Signaling Adaptor Proteins, Caspases, Initiator, Interleukin-1beta, Cryopyrin-Associated Periodic Syndromes, HEK293 Cells, Inflammasomes
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