Radon Improves Clinical Response in an Animal Model of Rheumatoid Arthritis Accompanied by Increased Numbers of Peripheral Blood B Cells and Interleukin-5 Concentration.
B cells
T cells
anti-oxidative system
immune system
inflammation
macrophages
monocytes
radon therapy
rheumatoid arthritis
serum transfer arthritis
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
16 02 2022
16 02 2022
Historique:
received:
23
12
2021
revised:
07
02
2022
accepted:
10
02
2022
entrez:
25
2
2022
pubmed:
26
2
2022
medline:
9
4
2022
Statut:
epublish
Résumé
Radon treatment is used as an established therapy option in chronic painful inflammatory diseases. While analgesic effects are well described, little is known about the underlying molecular effects. Among the suspected mechanisms are modulations of the anti-oxidative and the immune system. Therefore, we aimed for the first time to examine the beneficial effects of radon exposure on clinical outcome as well as the underlying mechanisms by utilizing a holistic approach in a controlled environment of a radon chamber with an animal model: K/BxN serum-induced arthritic mice as well as isolated cells were exposed to sham or radon irradiation. The effects on the anti-oxidative and the immune system were analyzed by flow-cytometry, qPCR or ELISA. We found a significantly improved clinical disease progression score in the mice, alongside significant increase of peripheral blood B cells and IL-5. No significant alterations were visible in the anti-oxidative system or regarding cell death. We conclude that neither cell death nor anti-oxidative systems are responsible for the beneficial effects of radon exposure in our preclinical model. Rather, radon slightly affects the immune system. However, more research is still needed in order to fully understand radon-mediated effects and to carry out reasonable risk-benefit considerations.
Identifiants
pubmed: 35203348
pii: cells11040689
doi: 10.3390/cells11040689
pmc: PMC8870723
pii:
doi:
Substances chimiques
Interleukin-5
0
Radon
Q74S4N8N1G
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Bundesministerium für Bildung und Forschung
ID : 02NUK017G, 02NUK050E, 02NUK050D, 02NUK050A
Organisme : Deutsche Forschungsgemeinschaft
ID : GK1660, CRC1181-A07, GK2886, GK2599
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