Alterations of monocyte NF-κB p65/RelA signaling in a cohort of older medical patients, age-matched controls, and healthy young adults

Altered monocyte NF-κB signaling is a possible cause of inflammaging and driver of aging, however, evidence from human aging studies is sparse. We assessed monocyte NF-κB signaling across different aging trajectories by comparing healthy older adults to older adults with a recent emergency departmen...

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Bibliographic Details
Published in:Immunity & ageing 2020-09, Vol.17 (1), p.25-25, Article 25
Main Authors: Tavenier, Juliette, Rasmussen, Line Jee Hartmann, Houlind, Morten Baltzer, Andersen, Aino Leegaard, Panum, Inge, Andersen, Ove, Petersen, Janne, Langkilde, Anne, Nehlin, Jan O
Format: Article
Language:English
Subjects:
Age
Aging
Antibodies
Bacterial infections
Cancer
Cell activation
Chronic illnesses
Chronic inflammation
Cognitive ability
Data collection
Emergency medical care
Flow cytometry
Frailty
Hospitalization
Hospitals
Immune response
Immunosenescence
Inflammaging
Inflammation
Interleukin 18
Interleukin 6
Lipopolysaccharides
Monocyte
Monocytes
Mortality
NF-κB
NF-κB protein
Older people
Patient admissions
Phosphorylation
Plasma levels
Senescence
Tumor necrosis factor-TNF
Tumor necrosis factor-α
U-Plasminogen activator
Vaccine efficacy
Young adults
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Summary:Altered monocyte NF-κB signaling is a possible cause of inflammaging and driver of aging, however, evidence from human aging studies is sparse. We assessed monocyte NF-κB signaling across different aging trajectories by comparing healthy older adults to older adults with a recent emergency department (ED) admission and to young adults. We used data from: 52 older (≥65 years) Patients collected upon ED admission and at follow-up 30-days after discharge; 52 age- and sex-matched Older Controls without recent hospitalization; and 60 healthy Young Controls (20-35 years). Using flow cytometry, we assessed basal NF-κB phosphorylation (pNF-κB p65/RelA; Ser529) and induction of pNF-κB following stimulation with LPS or TNF-α in monocytes. We assessed frailty (FI-OutRef), physical and cognitive function, and plasma levels of IL-6, IL-18, TNF-α, and soluble urokinase plasminogen activator receptor. Patients at follow-up were frailer, had higher levels of inflammatory markers and decreased physical and cognitive function than Older Controls. Patients at follow-up had higher basal pNF-κB levels than Older Controls (median fluorescence intensity (MFI): 125, IQR: 105-153 vs. MFI: 80, IQR: 71-90, p 
ISSN:1742-4933
1742-4933
DOI:10.1186/s12979-020-00197-7