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 journalArticle

21 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 languageEnglish
Pages (from-to)80-85
Number of pages6
JournalImmunology Letters
Volume154
Issue number1-2
DOIs
StatePublished - 2013 Jul 1

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Calcitriol
Myeloid Cells
Monocytes
Macrophages
RNA Stability
Cell Surface Receptors
Innate Immunity
Neutrophils
Messenger RNA
Proteins

Keywords

  • 1,25-Dihydroxyviamin D
  • Macrophages
  • Monocytes
  • TREM-1

Cite this

Kim, Tae-Hwan ; Lee, Bitnara ; Kwon, Eunji ; Choi, Sung Jae ; Lee, Young Ho ; Song, Gwan Gyu ; Sohn, Jeongwon ; Ji, Jong Dae. / Regulation of TREM-1 expression by 1,25-dihydroxyvitamin D3 in human monocytes/macrophages. In: Immunology Letters. 2013 ; Vol. 154, No. 1-2. pp. 80-85.
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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",
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Kim, T-H, Lee, B, Kwon, E, Choi, SJ, Lee, YH, Song, GG, Sohn, J & Ji, JD 2013, 'Regulation of TREM-1 expression by 1,25-dihydroxyvitamin D3 in human monocytes/macrophages', Immunology Letters, vol. 154, no. 1-2, pp. 80-85. https://doi.org/10.1016/j.imlet.2013.08.012

Regulation of TREM-1 expression by 1,25-dihydroxyvitamin D3 in human monocytes/macrophages. / Kim, Tae-Hwan; Lee, Bitnara; Kwon, Eunji; Choi, Sung Jae; Lee, Young Ho; Song, Gwan Gyu; Sohn, Jeongwon; Ji, Jong Dae.

In: Immunology Letters, Vol. 154, No. 1-2, 01.07.2013, p. 80-85.

Research output: Contribution to journalArticle

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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

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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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