Caffeine inhibits STAT1 signaling and downregulates inflammatory pathways involved in autoimmunity

Copyright © 2018 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 192(2018) vom: 01. Juli, Seite 68-77
1. Verfasser: Iris, Merve (VerfasserIn)
Weitere Verfasser: Tsou, Pei-Suen, Sawalha, Amr H
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2018
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Autoimmunity Caffeine Cytokine Inflammation Lupus Rheumatoid TNF Central Nervous System Stimulants Cytokines mehr... PPAR gamma PPARG protein, human STAT1 Transcription Factor STAT1 protein, human 3G6A5W338E
Beschreibung
Zusammenfassung:Copyright © 2018 Elsevier Inc. All rights reserved.
Caffeine is a widely consumed pharmacologically active product. We focused on characterizing immunomodulatory effects of caffeine on peripheral blood mononuclear cells. Caffeine at high doses showed a robust downregulatory effect on cytokine activity and genes related to several autoimmune diseases including lupus and rheumatoid arthritis. Dose-dependent validation experiments showed downregulation at the mRNA levels of key inflammation-related genes including STAT1, TNF, IFNG, and PPARG. TNF and PPARG were suppressed even with the lowest caffeine dose tested, which corresponds to the serum concentration of caffeine after administration of one cup of coffee. Cytokine levels of IL-8, MIP-1β, IL-6, IFN-γ, GM-CSF, TNF, IL-2, IL-4, MCP-1, and IL-10 were decreased significantly with caffeine treatment. Upstream regulator analysis suggests that caffeine inhibits STAT1 signaling, which was confirmed by showing reduced phosphorylated STAT1 after caffeine treatment. Further studies exploring disease-modulating potential of caffeine in autoimmune diseases and further exploring the mechanisms involved are warranted
Beschreibung:Date Completed 01.07.2019
Date Revised 01.07.2019
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2018.04.008