Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome
Open accessAbstract
Dying cells are capable of activating the innate immune system and inducing a sterile inflammatory response. Here, we show that necrotic cells are sensed by the Nlrp3 inflammasome resulting in the subsequent release of the proinflammatory cytokine IL-1β. Necrotic cells produced by pressure disruption, hypoxic injury, or complement-mediated damage were capable of activating the Nlrp3 inflammasome. Nlrp3 inflammasome activation was triggered in part through ATP produced by mitochondria released from damaged cells. Neutrophilic influx into the peritoneum in response to necrotic cells in vivo was also markedly diminished in the absence of Nlrp3. Nlrp3-deficiency moreover protected animals against mortality, renal dysfunction, and neutrophil influx in an in vivo renal ischemic acute tubular necrosis model. These findings suggest that the inhibition of Nlrp3 inflammasome activity can diminish the acute inflammation and damage associated with tissue injury.
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Necrotic cells can activate NLRP3, which is partly dependent on actively respiring mitochondria and the physiological release of ATP.
“Also, necrotic cells can activate NLRP3, which is partly dependent on actively respiring mitochondria and the physiological release of ATP60.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [60]
It is probable that additional factors besides ATP have a role in necrotic cell activation of NLRP3.
“It is probable that additional factors besides ATP have a role60.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [60]
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- Authors
- Iyer, S. S., Pulskens, W. P., Sadler, J. J., Butter, L. M., Teske, G. J., Ulland, T. K., Eisenbarth, S. C., Florquin, S., Flavell, R. A., Leemans, J. C., & Sutterwala, F. S.
- Affiliations
- University of Iowa (US)
- Amsterdam UMC Location University of Amsterdam (NL)
- Department of Laboratory Medicine,
- Howard Hughes Medical Institute (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-12
- Volume
- 106
- Issue
- 48
- Pages
- 20388-20393
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2787135
- OpenAlex
- W1992789370
- Cited by
- 691
- References
- 41
- Citations by year
- 2026: 13 · 2025: 23 · 2024: 38 · 2023: 26 · 2022: 39 · 2021: 33 · 2020: 42 · 2019: 30 · 2018: 50 · 2017: 36 · 2016: 59 · 2015: 40 · 2014: 75 · 2013: 69 · 2012: 52
- FWCI
- 15.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Heart, Lung, and Blood Institute (T32HL007974)
- National Institute of Allergy and Infectious Diseases (K08AI065517)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- NLRP3 inflammasome, sterile inflammation, necrosis, IL-1β, ATP release, mitochondrial ATP, neutrophil influx, acute tubular necrosis, renal ischemia, hypoxic injury
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Adenosine Triphosphate, Animals, Carrier Proteins, Enzyme-Linked Immunosorbent Assay, Inflammation, Mice, Inbred C57BL, Mitochondria, Necrosis, Extracellular Matrix Proteins, Mice, Interleukin-1beta
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