Expression of TREM-1 is inhibited by PGD2 and PGJ2 in macrophages |
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| Authors: | Mansoor Ali Syed M Joo D Rodger D Mehta |
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| Institution: | a Department of Veterans Affairs, Jesse Brown VA Hospital, University of Illinois at Chicago, Chicago, IL, USAb Section of Pulmonary, Critical Care, and Sleep Medicine, University of Illinois at Chicago, Chicago, IL, USAc Department of Pharmacology, University of Illinois at Chicago, Chicago, IL, USAd Pusan National University, Busan, Republic of Korea |
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| 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. |
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| Keywords: | Inflammation TREM-1 LPS Macrophage Prostaglandin PGD2 |
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