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TREM-1 expression in macrophages is regulated at transcriptional level by NF-kappaB and PU.1

Heng Zeng1, Magdalena Ornatowska, Myung S Joo

  • 1Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, and Department of Veterans Affairs, Jesse Brown VA Hospital, Chicago, IL 60612, USA.

European Journal of Immunology
|July 20, 2007
PubMed

Insights

This study reveals how the triggering receptor expressed on myeloid cells-1 (TREM-1) gene is regulated. Nuclear factor-kappa B (NF-κB) acts as a positive regulator, while PU.1 functions as a negative regulator in TREM-1 gene expression.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Triggering receptor expressed on myeloid cells-1 (TREM-1) is an immunoglobulin receptor found on neutrophils and monocytes.
  • TREM-1 amplifies the acute inflammatory response to bacterial infections.

Purpose of the Study:

  • To investigate the transcriptional regulation of TREM-1 in macrophages.
  • To elucidate the roles of NF-κB and PU.1 transcription factors in TREM-1 gene expression.

Main Methods:

  • RAW cells were treated with Escherichia coli lipopolysaccharide (LPS) or Pseudomonas aeruginosa.
  • TREM-1 expression was analyzed using RT-PCR.
  • NF-κB inhibitors were used to assess its role.
  • PU.1 gene silencing and overexpression were performed to evaluate its function.

Main Results:

  • LPS and P. aeruginosa induced TREM-1 expression within 1 hour, lasting up to 24 hours.
  • NF-κB inhibition abolished LPS- and P. aeruginosa-induced TREM-1 expression.
  • PU.1 silencing increased TREM-1 expression, while PU.1 overexpression inhibited it.

Conclusions:

  • NF-κB acts as a positive regulator of TREM-1 gene expression.
  • PU.1 acts as a negative regulator of TREM-1 gene expression.
  • Both NF-κB and PU.1 are critical in regulating TREM-1 transcription in response to bacterial stimuli.

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