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Dexamethasone Down-Regulates Expression of Triggering Receptor Expressed on Myeloid Cells-1: Evidence for a

Ira Mihailidou1, Aimilia Pelekanou1, Aikaterini Pistiki1

  • 14th Department of Internal Medicine, University of Athens Medical School , Athens , Greece.

Frontiers in Public Health
|December 19, 2013
PubMed
Abstract

Insights

Dexamethasone prolonged survival in mice infected with Pseudomonas aeruginosa by down-regulating triggering receptor expressed on myeloid cells-1 (TREM-1). This effect, mediated by TNFα, highlights TREM-1 as a novel target for dexamethasone action.

Area of Science:

  • Immunology
  • Pharmacology
  • Infectious Diseases

Background:

  • Triggering receptor expressed on myeloid cells-1 (TREM-1) plays a role in inflammatory responses.
  • The impact of corticosteroids like dexamethasone on TREM-1 expression and function remains incompletely understood.

Purpose of the Study:

  • To investigate the effect of dexamethasone on TREM-1 expression and its role in bacterial infection models.
  • To elucidate the mechanisms underlying dexamethasone's action on TREM-1, including the involvement of TNFα.

Main Methods:

  • Animal models (wild-type and TNF knockout mice) infected with Pseudomonas aeruginosa were treated with dexamethasone or hydrocortisone.
  • Mortality, neutrophil TREM-1 expression, and soluble TREM-1 (sTREM-1) levels were assessed.
  • In vitro studies using U937 monocytic cells stimulated with LPS or P. aeruginosa were performed with or without dexamethasone/hydrocortisone, and in the presence/absence of TNFα or anti-TNFα antibody.

Main Results:

  • Dexamethasone, but not hydrocortisone, improved survival in infected mice and reduced neutrophil TREM-1 expression.
  • Dexamethasone suppressed LPS- or P. aeruginosa-induced TREM-1 and sTREM-1 expression in U937 cells.
  • The suppressive effect of dexamethasone was dependent on TNFα, as it was enhanced by exogenous TNFα and lost with anti-TNFα antibody or in TNF knockout mice.

Conclusions:

  • TREM-1/sTREM-1 represents a novel site of action for dexamethasone.
  • Dexamethasone down-regulates TREM-1 gene expression.
  • The anti-TREM-1 effects of dexamethasone are mediated through a TNFα-dependent pathway.
Keywords:
Pseudomonas aeruginosaTNFαTREM-1dexamethasonemonocytes

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