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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López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues
Swerdlow, S. H. (2017) · Medical Entomology and Zoology · Cited by 12,933
Arber, D. A., Orazi, A., Hasserjian, R., Thiele, J., Borowitz, M. J., Le Beau, M. M., Bloomfield, C. D., Cazzola, M., & Vardiman, J. W. (2016) · Blood · doi:10.1182/blood-2016-03-643544 · Cited by 10,119
Inflamm‐aging: An Evolutionary Perspective on Immunosenescence
FRANCESCHI, C., BONAFÈ, M., VALENSIN, S., OLIVIERI, F., DE LUCA, M., OTTAVIANI, E., & DE BENEDICTIS, G. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb06651.x · Cited by 5,358
The NLRP3 inflammasome: molecular activation and regulation to therapeutics
Swanson, K. V., Deng, M., & Ting, J. P.-Y. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0165-0 · Cited by 4,884
Age-related clonal hematopoiesis associated with adverse outcomes
Jaiswal, S., Fontanillas, P., Flannick, J., Manning, A., Grauman, P. V., Mar, B. G., Lindsley, R. C., Mermel, C. H., Burtt, N., Chavez, A., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1408617 · Cited by 4,841
International scoring system for evaluating prognosis in myelodysplastic syndromes
Greenberg, P., Cox, C., LeBeau, M. M., Fenaux, P., Morel, P., Sanz, G., Sanz, M., Vallespi, T., Hamblin, T., Oscier, D., et al. (1997) · Blood · doi:10.1182/blood.v89.6.2079 · Cited by 4,427
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
Duewell, P., Kono, H., Rayner, K. J., Sirois, C. M., Vladimer, G., Bauernfeind, F. G., Abela, G. S., Franchi, L., Nuñez, G., Schnurr, M., et al. (2010) · Nature · doi:10.1038/nature08938 · Cited by 4,026
Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty
Ferrucci, L., & Fabbri, E. (2018) · Nature Reviews Cardiology · doi:10.1038/s41569-018-0064-2 · Cited by 3,690
Inflammaging: a new immune–metabolic viewpoint for age-related diseases
Franceschi, C., Garagnani, P., Parini, P., Giuliani, C., & Santoro, A. (2018) · Nature Reviews Endocrinology · doi:10.1038/s41574-018-0059-4 · Cited by 3,586
Research works printed but not linked: 2
- Wu, 2018, Impact of proteasome inhibitor MG-132 on expression of NF-κB, IL-1β and histological remodeling after myocardial infarction, Exp. Ther. Med., 16, 1365
- Kale, 2011, Effects of aging on inflammation and hemostasis through the continuum of critical illness, Aging Dis., 2, 501
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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