Chronic Inflammation Disrupts Circadian Rhythms in Splenic CD4+ and CD8+ T Cells in Mice.
CD4+ T cells
CD8+ T cells
circadian clock
complete Freund’s adjuvant (CFA)
experimental autoimmune encephalomyelitis (EAE)
inflammation
pertussis toxin (PTx)
spleen
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
13 Jan 2024
13 Jan 2024
Historique:
received:
07
12
2023
revised:
10
01
2024
accepted:
11
01
2024
medline:
22
1
2024
pubmed:
22
1
2024
entrez:
22
1
2024
Statut:
epublish
Résumé
Internal circadian clocks coordinate 24 h rhythms in behavior and physiology. Many immune functions show daily oscillations, and cellular circadian clocks can impact immune functions and disease outcome. Inflammation may disrupt circadian clocks in peripheral tissues and innate immune cells. However, it remains elusive if chronic inflammation impacts adaptive immune cell clock, e.g., in CD4+ and CD8+ T lymphocytes. We studied this in the experimental autoimmune encephalomyelitis (EAE), a mouse model for multiple sclerosis, as an established experimental paradigm for chronic inflammation. We analyzed splenic T cell circadian clock and immune gene expression rhythms in mice with late-stage EAE, CFA/PTx-treated, and untreated mice. In both treatment groups, clock gene expression rhythms were altered with differential effects for baseline expression and peak phase compared with control mice. Most immune cell marker genes tested in this study did not show circadian oscillations in either of the three groups, but time-of-day- independent alterations were observed in EAE and CFA/PTx compared to control mice. Notably, T cell effects were likely independent of central clock function as circadian behavioral rhythms in EAE mice remained intact. Together, chronic inflammation induced by CFA/PTx treatment and EAE immunization has lasting effects on circadian rhythms in peripheral immune cells.
Identifiants
pubmed: 38247842
pii: cells13020151
doi: 10.3390/cells13020151
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB-296 TP13 & HO353-10/1
Organisme : Volkswagen Foundation
ID : Lichtenberg Program