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Cited by 16

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

Andina, Nicola, de Meuron, Louise, Schnegg-Kaufmann, Annatina Sarah, Sarangdhar, Mayuresh Anant, Ansermet, Camille, Bombaci, Giuseppe, Batta, Kiran, Keller, Nino, Porret, Naomi A, Angelillo-Scherrer, Anne, Bonadies, Nicolas, Allam, Ramanjaneyulu·2023·The Journal of Immunology
DOI 10.4049/jimmunol.2200412
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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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Research works printed but not linked: 2

  1. 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
  2. Kale, 2011, Effects of aging on inflammation and hemostasis through the continuum of critical illness, Aging Dis., 2, 501

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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
DOI
10.4049/jimmunol.2200412
Cited by
16
References
63
Language
en
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Funders
  • Novartis Stiftung für Medizinisch-Biologische Forschung
  • Olga Mayenfisch Stiftung

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