Glutathione Metabolism Contributes to the Induction of Trained Immunity.
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Authors
Ferreira, Anaisa VKoeken, Valerie A C M
Matzaraki, Vasiliki
Kostidis, Sarantos
Alarcon-Barrera, Juan Carlos
de Bree, L Charlotte J
Moorlag, Simone J C F M
Mourits, Vera P
Novakovic, Boris
Giera, Martin A
Netea, Mihai G
Domínguez-Andrés, Jorge
Issue Date
2021-04-21
Metadata
Show full item recordAbstract
The innate immune system displays heterologous memory characteristics, which are characterized by stronger responses to a secondary challenge. This phenomenon termed trained immunity relies on epigenetic and metabolic rewiring of innate immune cells. As reactive oxygen species (ROS) production has been associated with the trained immunity phenotype, we hypothesized that the increased ROS levels and the main intracellular redox molecule glutathione play a role in the induction of trained immunity. Here we show that pharmacological inhibition of ROS in an in vitro model of trained immunity did not influence cell responsiveness; the modulation of glutathione levels reduced pro-inflammatory cytokine production in human monocytes. Single nucleotide polymorphisms (SNPs) in genes involved in glutathione metabolism were found to be associated with changes in pro-inflammatory cytokine production capacity upon trained immunity. Also, plasma glutathione concentrations were positively associated with ex vivo IL-1β production, a biomarker of trained immunity, produced by monocytes of BCG-vaccinated individuals. In conclusion, glutathione metabolism is involved in the induction of trained immunity, and future studies are warranted to explore its functional consequences in human diseases.Citation
Cells. 2021 Apr 21;10(5):971. doi: 10.3390/cells10050971.Affiliation
CiiM, Zentrum für individualisierte Infektionsmedizin, Feodor-Lynen-Str.7, 30625 Hannover.Publisher
MDPIJournal
CellsPubMed ID
33919212Type
ArticleLanguage
enEISSN
2073-4409ae974a485f413a2113503eed53cd6c53
10.3390/cells10050971
Scopus Count
The following license files are associated with this item:
- Creative Commons