The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
Increased Inflammasome Activation Is Associated with Aging and Chronic Myelomonocytic Leukemia Disease Severity
Abstract
Aging causes chronic low-grade inflammation known as inflamm-aging. It is a risk factor for several chronic disorders, including chronic myelomonocytic leukemia (CMML), a hematological malignancy that is most prevalent in older people. Recent studies suggest a critical role for the NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome in inflamm-aging. However, the mechanisms involved in NLRP3 activation in aging and its involvement in CMML progression are not fully understood. In this study, we report that aging increases IL-1β production upon NLRP3 activation in human CD14+ monocytes. Interestingly, we found that the TLR1/2 agonist Pam3CSK4 directly activates the NLRP3 inflammasome in monocytes from older but not from younger healthy donors. Furthermore, we observed a dichotomous response to NLRP3 inflammasome activation in monocytes from a small cohort of CMML patients, and some patients produced high levels of IL-1β and some patients produced low levels of IL-1β compared with older healthy donors. Intriguingly, CMML patients with heightened NLRP3 activation showed increased treatment dependency and disease severity. Collectively, our results suggest that aging causes increased sensitivity to NLRP3 inflammasome activation at a cellular level, which may explain increased inflammation and immune dysregulation in older individuals. Furthermore, NLRP3 inflammasome activation was dysregulated in a small cohort of CMML patients and was positively correlated with disease severity.
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“Several studies have shown that ageing haematopoietic stem cells (HSCs) upregulate NLRP3 inflammasome activity.”
From Clonal haematopoiesis and dysregulation of the immune system (2023) · cites this paper as [200]
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“Aged HSCs demonstrate heightened NLRP3-dependent inflammatory responses to lipopolysaccharide and ATP stimulation compared with young HSCs due to increased mitochondrial oxidative stress 200 .”
From Clonal haematopoiesis and dysregulation of the immune system (2023) · cites this paper as [200]
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Inflamm‐aging: An Evolutionary Perspective on Immunosenescence
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The NLRP3 inflammasome: molecular activation and regulation to therapeutics
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NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
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Cited by
Chronic inflammation and the hallmarks of aging
Baechle, J. J., Chen, N., Makhijani, P., Winer, S., Furman, D., & Winer, D. A. (2023) · Molecular Metabolism · doi:10.1016/j.molmet.2023.101755 · Cited by 471
Clonal haematopoiesis and dysregulation of the immune system
Belizaire, R., Wong, W. J., Robinette, M. L., & Ebert, B. L. (2023) · Nature Reviews Immunology · doi:10.1038/s41577-023-00843-3 · Cited by 161
Metadata
- Authors
- Andina, N., de Meuron, L., Schnegg-Kaufmann, A. S., Sarangdhar, M. A., Ansermet, C., Bombaci, G., Batta, K., Keller, N., Porret, N. A., Angelillo-Scherrer, A., Bonadies, N., & Allam, R.
- Affiliations
- Department of Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern , Bern,
- Epigenetics of Haematopoiesis Laboratory, Division of Cancer Sciences, The University of Manchester , Manchester,
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2023-01-20
- Volume
- 210
- Issue
- 5
- Pages
- 580-589
- ISSN
- 0022-1767
- 1550-6606
- Cited by
- 16
- References
- 63
- Language
- en
- Funders
- Novartis Stiftung für Medizinisch-Biologische Forschung
- Olga Mayenfisch Stiftung
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- Andina, N., de Meuron, L., Schnegg-Kaufmann, A. S., Sarangdhar, M. A., Ansermet, C., Bombaci, G., Batta, K., Keller, N., Porret, N. A., Angelillo-Scherrer, A., Bonadies, N., & Allam, R. (2023). Increased Inflammasome Activation Is Associated with Aging and Chronic Myelomonocytic Leukemia Disease Severity. The Journal of Immunology. https://doi.org/10.4049/jimmunol.2200412
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
