The Aging Process Alters IL-1β and CD63 Levels Differently in Extracellular Vesicles Obtained from the Plasma and Cerebrospinal Fluid

Objective(s): The aim of this study was to investigate exosomal markers and inflammatory cargo of extracellular vesicles (EVs) obtained from cerebrospinal fluid (CSF) and plasma in the aging process. We also studied the inflammatory cargo by quantifying IL-1β levels. Methods: Male Wistar rats, aged...

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Veröffentlicht in:Neuroimmunomodulation 2018-01, Vol.25 (1), p.18-22
Hauptverfasser: Gomes de Andrade, Gisele, Reck Cechinel, Laura, Bertoldi, Karine, Galvão, Fernando, Valdeci Worm, Paulo, Rodrigues Siqueira, Ionara
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Sprache:eng
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Zusammenfassung:Objective(s): The aim of this study was to investigate exosomal markers and inflammatory cargo of extracellular vesicles (EVs) obtained from cerebrospinal fluid (CSF) and plasma in the aging process. We also studied the inflammatory cargo by quantifying IL-1β levels. Methods: Male Wistar rats, aged 3 and 21 months, were used (n = 12 in each group). The CSF and plasma of animals were collected, and isolation of EVs was performed using a commercial kit. Total protein concentration, acetylcholinesterase (AChE) activity, and CD63 and IL-1β levels were evaluated. Results: AChE activity in EVs increased in both samples, specifically in the circulating EVs and those in the CSF of the older group. An age-related increase was observed in CD63 levels in EVs from the CSF but a decrease was observed in plasma EVs of the older group. Student’s t test showed that the young adult rats had significantly higher circulating IL-1β levels in the EVs compared to the aged ones, without any effect on central content. Conclusion: Our data suggest that the normal aging process causes different changes in the profiles of central and circulating EVs. Altered IL-1β levels in circulating EVs can be linked, at least partly, to age-related inflammatory conditions, and a disruption of the CFS exosomes in aged rats, evaluated by CD63 levels, can be related to susceptibility to neurodegenerative disorders.
ISSN:1021-7401
1423-0216
DOI:10.1159/000488943