Regulation of TREM-1 expression by 1,25-dihydroxyvitamin D3 in human monocytes/macrophages

Tae Hwan Kim; Bitnara Lee; Eunji Kwon; Sung Jae Choi; Young Ho Lee; Gwan Gyu Song; Jeongwon Sohn; Jong Dae Ji

doi:10.1016/j.imlet.2013.08.012

Regulation of TREM-1 expression by 1,25-dihydroxyvitamin D₃ in human monocytes/macrophages

Tae Hwan Kim, Bitnara Lee, Eunji Kwon, Sung Jae Choi, Young Ho Lee, Gwan Gyu Song, Jeongwon Sohn, Jong Dae Ji

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

32 Citations (Scopus)

Abstract

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and acts as an amplifier of immune responses. In this study, 1,25(OH)₂D₃ strongly upregulated the expression of TREM-1 in human monocytes and macrophages. 1,25(OH)₂D₃ stimulated TREM-1 mRNA expression by augmenting transcription, and not by inhibiting mRNA degradation. The upregulated expression of TREM-1 by 1,25(OH)₂D₃ was dependent on the NF-κB signaling pathway and required new protein synthesis in differentiated U937 macrophages. Our results show that 1,25(OH)₂D₃ can affect the innate and inflammatory responses by upregulating TREM-1 expression, and suggest that 1,25(OH)₂D₃ may function as an enhancer of the innate immune response by upregulating TREM-1 expression, in addition to inducing the antimicrobial peptide cathelicidin.

Original language	English
Pages (from-to)	80-85
Number of pages	6
Journal	Immunology Letters
Volume	154
Issue number	1-2
DOIs	https://doi.org/10.1016/j.imlet.2013.08.012
Publication status	Published - 2013 Jul
Externally published	Yes

Bibliographical note

Funding Information:
This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology ( 2012R1A1A2001950 to J.D.J) and ( 2010-0022379 T-H.K).

Keywords

1,25-Dihydroxyviamin D
Macrophages
Monocytes
TREM-1

ASJC Scopus subject areas

Immunology and Allergy
Immunology

Access to Document

10.1016/j.imlet.2013.08.012

Cite this

@article{ef743fd1e51045f497632336779b45d1,

title = "Regulation of TREM-1 expression by 1,25-dihydroxyvitamin D3 in human monocytes/macrophages",

abstract = "Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and acts as an amplifier of immune responses. In this study, 1,25(OH)2D3 strongly upregulated the expression of TREM-1 in human monocytes and macrophages. 1,25(OH)2D3 stimulated TREM-1 mRNA expression by augmenting transcription, and not by inhibiting mRNA degradation. The upregulated expression of TREM-1 by 1,25(OH)2D3 was dependent on the NF-κB signaling pathway and required new protein synthesis in differentiated U937 macrophages. Our results show that 1,25(OH)2D3 can affect the innate and inflammatory responses by upregulating TREM-1 expression, and suggest that 1,25(OH)2D3 may function as an enhancer of the innate immune response by upregulating TREM-1 expression, in addition to inducing the antimicrobial peptide cathelicidin.",

keywords = "1,25-Dihydroxyviamin D, Macrophages, Monocytes, TREM-1",

author = "Kim, {Tae Hwan} and Bitnara Lee and Eunji Kwon and Choi, {Sung Jae} and Lee, {Young Ho} and Song, {Gwan Gyu} and Jeongwon Sohn and Ji, {Jong Dae}",

note = "Funding Information: This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology ( 2012R1A1A2001950 to J.D.J) and ( 2010-0022379 T-H.K).",

year = "2013",

month = jul,

doi = "10.1016/j.imlet.2013.08.012",

language = "English",

volume = "154",

pages = "80--85",

journal = "Immunology Letters",

issn = "0165-2478",

publisher = "Elsevier B.V.",

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T1 - Regulation of TREM-1 expression by 1,25-dihydroxyvitamin D3 in human monocytes/macrophages

AU - Kim, Tae Hwan

AU - Lee, Bitnara

AU - Kwon, Eunji

AU - Choi, Sung Jae

AU - Lee, Young Ho

AU - Song, Gwan Gyu

AU - Sohn, Jeongwon

AU - Ji, Jong Dae

N1 - Funding Information: This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology ( 2012R1A1A2001950 to J.D.J) and ( 2010-0022379 T-H.K).

PY - 2013/7

Y1 - 2013/7

N2 - Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and acts as an amplifier of immune responses. In this study, 1,25(OH)2D3 strongly upregulated the expression of TREM-1 in human monocytes and macrophages. 1,25(OH)2D3 stimulated TREM-1 mRNA expression by augmenting transcription, and not by inhibiting mRNA degradation. The upregulated expression of TREM-1 by 1,25(OH)2D3 was dependent on the NF-κB signaling pathway and required new protein synthesis in differentiated U937 macrophages. Our results show that 1,25(OH)2D3 can affect the innate and inflammatory responses by upregulating TREM-1 expression, and suggest that 1,25(OH)2D3 may function as an enhancer of the innate immune response by upregulating TREM-1 expression, in addition to inducing the antimicrobial peptide cathelicidin.

AB - Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and acts as an amplifier of immune responses. In this study, 1,25(OH)2D3 strongly upregulated the expression of TREM-1 in human monocytes and macrophages. 1,25(OH)2D3 stimulated TREM-1 mRNA expression by augmenting transcription, and not by inhibiting mRNA degradation. The upregulated expression of TREM-1 by 1,25(OH)2D3 was dependent on the NF-κB signaling pathway and required new protein synthesis in differentiated U937 macrophages. Our results show that 1,25(OH)2D3 can affect the innate and inflammatory responses by upregulating TREM-1 expression, and suggest that 1,25(OH)2D3 may function as an enhancer of the innate immune response by upregulating TREM-1 expression, in addition to inducing the antimicrobial peptide cathelicidin.

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