Retinol suppresses the activation of toll-like receptors in MyD88- and STAT1-independent manners

So Young Kim; Jung Eun Koo; Mi Ryoung Song; Joo Young Lee

doi:10.1007/s10753-012-9562-2

Retinol suppresses the activation of toll-like receptors in MyD88- and STAT1-independent manners

So Young Kim
, Jung Eun Koo
, Mi Ryoung Song
, Joo Young Lee

Gwangju Institute of Science and Technology
The Catholic University of Korea

Research output: Contribution to journal › Article › peer-review

17 Scopus citations

Abstract

Dysregulation of Toll-like receptor (TLR) activation is well known to be linked to development and aggravation of inflammatory diseases and immune disorders. Retinol is reported to participate in regulation of immune responses. However, it has not been fully understood how retinol regulates TLR activation in macrophages. Our results showed that retinol suppressed the expression of various inflammatory cytokines in bone marrow-derived macrophages stimulated with ligands of TLR2, TLR3, or TLR4. These demonstrate that inhibitory effect of retinol is not limited to a single TLR. Inhibitory effect of retinol on lipopolysaccharide-induced target gene expression was still observed in myeloid differentiation primary-response protein 88 (MyD88)- or signal transducer and activator of transcription 1 (STAT1)-deficient macrophages, indicating that MyD88 and STAT1 are dispensable for retinol-mediated blockade of TLRs. Together, the results demonstrate that retinol suppresses the activation of TLRs in macrophages resulting in downregulation of inflammatory gene expression and further suggest that beneficial effect of retinol is mediated through regulation of TLR-mediated inflammatory responses.

Original language	English
Pages (from-to)	426-433
Number of pages	8
Journal	Inflammation
Volume	36
Issue number	2
DOIs	https://doi.org/10.1007/s10753-012-9562-2
State	Published - Apr 2013

Bibliographical note

Funding Information:
We thank Young Ju Lim and Yoon Sun Kim for their technical assistance. This study was supported by a grant from Cell Dynamics Research Center, National Research Foundation of Korea (2012–0000766), a grant from Korea Institute of Oriental Medicine (Grant No. K12080), and the Research Fund, 2012 of the Catholic University of Korea.

Keywords

inflammatory genes
macrophages
retinol
toll-like receptors

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10.1007/s10753-012-9562-2

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title = "Retinol suppresses the activation of toll-like receptors in MyD88- and STAT1-independent manners",

abstract = "Dysregulation of Toll-like receptor (TLR) activation is well known to be linked to development and aggravation of inflammatory diseases and immune disorders. Retinol is reported to participate in regulation of immune responses. However, it has not been fully understood how retinol regulates TLR activation in macrophages. Our results showed that retinol suppressed the expression of various inflammatory cytokines in bone marrow-derived macrophages stimulated with ligands of TLR2, TLR3, or TLR4. These demonstrate that inhibitory effect of retinol is not limited to a single TLR. Inhibitory effect of retinol on lipopolysaccharide-induced target gene expression was still observed in myeloid differentiation primary-response protein 88 (MyD88)- or signal transducer and activator of transcription 1 (STAT1)-deficient macrophages, indicating that MyD88 and STAT1 are dispensable for retinol-mediated blockade of TLRs. Together, the results demonstrate that retinol suppresses the activation of TLRs in macrophages resulting in downregulation of inflammatory gene expression and further suggest that beneficial effect of retinol is mediated through regulation of TLR-mediated inflammatory responses.",

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note = "Funding Information: We thank Young Ju Lim and Yoon Sun Kim for their technical assistance. This study was supported by a grant from Cell Dynamics Research Center, National Research Foundation of Korea (2012–0000766), a grant from Korea Institute of Oriental Medicine (Grant No. K12080), and the Research Fund, 2012 of the Catholic University of Korea.",

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AU - Song, Mi Ryoung

AU - Lee, Joo Young

N1 - Funding Information: We thank Young Ju Lim and Yoon Sun Kim for their technical assistance. This study was supported by a grant from Cell Dynamics Research Center, National Research Foundation of Korea (2012–0000766), a grant from Korea Institute of Oriental Medicine (Grant No. K12080), and the Research Fund, 2012 of the Catholic University of Korea.

PY - 2013/4

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N2 - Dysregulation of Toll-like receptor (TLR) activation is well known to be linked to development and aggravation of inflammatory diseases and immune disorders. Retinol is reported to participate in regulation of immune responses. However, it has not been fully understood how retinol regulates TLR activation in macrophages. Our results showed that retinol suppressed the expression of various inflammatory cytokines in bone marrow-derived macrophages stimulated with ligands of TLR2, TLR3, or TLR4. These demonstrate that inhibitory effect of retinol is not limited to a single TLR. Inhibitory effect of retinol on lipopolysaccharide-induced target gene expression was still observed in myeloid differentiation primary-response protein 88 (MyD88)- or signal transducer and activator of transcription 1 (STAT1)-deficient macrophages, indicating that MyD88 and STAT1 are dispensable for retinol-mediated blockade of TLRs. Together, the results demonstrate that retinol suppresses the activation of TLRs in macrophages resulting in downregulation of inflammatory gene expression and further suggest that beneficial effect of retinol is mediated through regulation of TLR-mediated inflammatory responses.

AB - Dysregulation of Toll-like receptor (TLR) activation is well known to be linked to development and aggravation of inflammatory diseases and immune disorders. Retinol is reported to participate in regulation of immune responses. However, it has not been fully understood how retinol regulates TLR activation in macrophages. Our results showed that retinol suppressed the expression of various inflammatory cytokines in bone marrow-derived macrophages stimulated with ligands of TLR2, TLR3, or TLR4. These demonstrate that inhibitory effect of retinol is not limited to a single TLR. Inhibitory effect of retinol on lipopolysaccharide-induced target gene expression was still observed in myeloid differentiation primary-response protein 88 (MyD88)- or signal transducer and activator of transcription 1 (STAT1)-deficient macrophages, indicating that MyD88 and STAT1 are dispensable for retinol-mediated blockade of TLRs. Together, the results demonstrate that retinol suppresses the activation of TLRs in macrophages resulting in downregulation of inflammatory gene expression and further suggest that beneficial effect of retinol is mediated through regulation of TLR-mediated inflammatory responses.

KW - inflammatory genes

KW - macrophages

KW - retinol

KW - toll-like receptors

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SN - 0360-3997

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JO - Inflammation

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IS - 2

ER -

Retinol suppresses the activation of toll-like receptors in MyD88- and STAT1-independent manners

Abstract

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Keywords

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