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2017 ; 8
(ä): 1239
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Glutathione Fine-Tunes the Innate Immune Response toward Antiviral Pathways in a
Macrophage Cell Line Independently of Its Antioxidant Properties
#MMPMID29033950
Diotallevi M
; Checconi P
; Palamara AT
; Celestino I
; Coppo L
; Holmgren A
; Abbas K
; Peyrot F
; Mengozzi M
; Ghezzi P
Front Immunol
2017[]; 8
(ä): 1239
PMID29033950
show ga
Glutathione (GSH), a major cellular antioxidant, is considered an inhibitor of
the inflammatory response involving reactive oxygen species (ROS). However,
evidence is largely based on experiments with exogenously added
antioxidants/reducing agents or pro-oxidants. We show that depleting macrophages
of 99% of GSH does not exacerbate the inflammatory gene expression profile in the
RAW264 macrophage cell line or increase expression of inflammatory cytokines in
response to the toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS);
only two small patterns of LPS-induced genes were sensitive to GSH depletion. One
group, mapping to innate immunity and antiviral responses (Oas2, Oas3, Mx2, Irf7,
Irf9, STAT1, il1b), required GSH for optimal induction. Consequently, GSH
depletion prevented the LPS-induced activation of antiviral response and its
inhibition of influenza virus infection. LPS induction of a second group of genes
(Prdx1, Srxn1, Hmox1, GSH synthase, cysteine transporters), mapping to nrf2 and
the oxidative stress response, was increased by GSH depletion. We conclude that
the main function of endogenous GSH is not to limit inflammation but to fine-tune
the innate immune response to infection.
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