Expression of TREM-1 is inhibited by PGD2 and PGJ2 in macrophages

Mansoor Ali Syed, M. Joo, Zulfiqar Abbas, D. Rodger, J. W. Christman, D. Mehta, R. T. Sadikot

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

TREM-1 is a superimmunoglobulin receptor present on neutrophils and monocytes, which plays an important role in the amplification of inflammation. The natural ligands for TREM-1 have not been identified; however, Toll-like receptor ligands are known to induce the expression of TREM-1. Blockade of TREM-1 has shown to improve survival in animal models of sepsis. In the present studies, we investigated the role of lipid mediators in the expression of TREM-1. In a macrophage cell line, we show that the expression of TREM-1 in response to LPS and bacteria Pseudomonas aeruginosa is inhibited by PGD2 and cyclopentanone prostaglandins PGJ2 and 15-dPGJ2. The inhibition of TREM-1 by these prostaglandins is independent of the PGD2 receptors and PPARγ but occurs by activation of Nrf2 and inhibition of NF-κB. Our data suggest a novel mechanism by which these prostaglandins exhibit anti-inflammatory effects and a new therapeutic approach to inhibition of TREM-1.

Original languageEnglish (US)
Pages (from-to)3140-3149
Number of pages10
JournalExperimental Cell Research
Volume316
Issue number19
DOIs
StatePublished - Nov 15 2010
Externally publishedYes

Keywords

  • Inflammation
  • LPS
  • Macrophage
  • Prostaglandin
  • TREM-1

ASJC Scopus subject areas

  • Cell Biology

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