Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo

Abstract Post-translational redox modification of methionine residues often triggers a change in protein function. Emerging evidence points to this reversible protein modification being an important regulatory mechanism under various physiological conditions. Reduction of oxidized methionine residue...

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Autores principales:	Byung Cheon Lee, Sang-Goo Lee, Min-Kyung Choo, Ji Hyung Kim, Hae Min Lee, Sorah Kim, Dmitri E. Fomenko, Hwa-Young Kim, Jin Mo Park, Vadim N. Gladyshev
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/32e6039149734ba7867298af541fc4fb
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spelling	oai:doaj.org-article:32e6039149734ba7867298af541fc4fb2021-12-02T12:30:52ZSelenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo10.1038/s41598-017-05230-22045-2322https://doaj.org/article/32e6039149734ba7867298af541fc4fb2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05230-2https://doaj.org/toc/2045-2322Abstract Post-translational redox modification of methionine residues often triggers a change in protein function. Emerging evidence points to this reversible protein modification being an important regulatory mechanism under various physiological conditions. Reduction of oxidized methionine residues is catalyzed by methionine sulfoxide reductases (Msrs). Here, we show that one of these enzymes, a selenium-containing MsrB1, is highly expressed in immune-activated macrophages and contributes to shaping cellular and organismal immune responses. In particular, lipopolysaccharide (LPS) induces expression of MsrB1, but not other Msrs. Genetic ablation of MsrB1 did not preclude LPS-induced intracellular signaling in macrophages, but resulted in attenuated induction of anti-inflammatory cytokines, such as interleukin (IL)-10 and the IL-1 receptor antagonist. This anomaly was associated with excessive pro-inflammatory cytokine production as well as an increase in acute tissue inflammation in mice. Together, our findings suggest that MsrB1 controls immune responses by promoting anti-inflammatory cytokine expression in macrophages. MsrB1-dependent reduction of oxidized methionine in proteins may be a heretofore unrecognized regulatory event underlying immunity and inflammatory disease, and a novel target for clinical applications.Byung Cheon LeeSang-Goo LeeMin-Kyung ChooJi Hyung KimHae Min LeeSorah KimDmitri E. FomenkoHwa-Young KimJin Mo ParkVadim N. GladyshevNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Byung Cheon Lee Sang-Goo Lee Min-Kyung Choo Ji Hyung Kim Hae Min Lee Sorah Kim Dmitri E. Fomenko Hwa-Young Kim Jin Mo Park Vadim N. Gladyshev Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo
description	Abstract Post-translational redox modification of methionine residues often triggers a change in protein function. Emerging evidence points to this reversible protein modification being an important regulatory mechanism under various physiological conditions. Reduction of oxidized methionine residues is catalyzed by methionine sulfoxide reductases (Msrs). Here, we show that one of these enzymes, a selenium-containing MsrB1, is highly expressed in immune-activated macrophages and contributes to shaping cellular and organismal immune responses. In particular, lipopolysaccharide (LPS) induces expression of MsrB1, but not other Msrs. Genetic ablation of MsrB1 did not preclude LPS-induced intracellular signaling in macrophages, but resulted in attenuated induction of anti-inflammatory cytokines, such as interleukin (IL)-10 and the IL-1 receptor antagonist. This anomaly was associated with excessive pro-inflammatory cytokine production as well as an increase in acute tissue inflammation in mice. Together, our findings suggest that MsrB1 controls immune responses by promoting anti-inflammatory cytokine expression in macrophages. MsrB1-dependent reduction of oxidized methionine in proteins may be a heretofore unrecognized regulatory event underlying immunity and inflammatory disease, and a novel target for clinical applications.
format	article
author	Byung Cheon Lee Sang-Goo Lee Min-Kyung Choo Ji Hyung Kim Hae Min Lee Sorah Kim Dmitri E. Fomenko Hwa-Young Kim Jin Mo Park Vadim N. Gladyshev
author_facet	Byung Cheon Lee Sang-Goo Lee Min-Kyung Choo Ji Hyung Kim Hae Min Lee Sorah Kim Dmitri E. Fomenko Hwa-Young Kim Jin Mo Park Vadim N. Gladyshev
author_sort	Byung Cheon Lee
title	Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo
title_short	Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo
title_full	Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo
title_fullStr	Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo
title_full_unstemmed	Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo
title_sort	selenoprotein msrb1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/32e6039149734ba7867298af541fc4fb
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Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo

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