International Immunology Advance Access originally published online on November 10, 2006
International Immunology 2007 19(1):41-50; doi:10.1093/intimm/dxl119
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Effects of TREM-1 activation in human neutrophils: activation of signaling pathways, recruitment into lipid rafts and association with TLR4
1 Immunology Graduate Program, Clinical Research Center, Faculty of Medicine, University of Sherbrooke, Québec J1H 4C4, Canada
2 Department of Medicine, Pneumology Division, University of Sherbrooke, Québec J1H 4C4, Canada
3 Department of Medicine, Geriatrics Division, Faculty of Medicine, University of Sherbrooke, Québec J1H 4C4, Canada
4 Present address: Laboratory of Immunology, Research Center on Aging, University of Sherbrooke, 1036 rue Belvédère sud Sherbrooke, Québec J1H 4C4, Canada
Correspondence to: T. Fulop Jr; E-mail: tamas.fulop{at}usherbrooke.ca
Neutrophilic polymorphonuclears (PMNs) play an important role in the progression of sepsis-related inflammation and become highly activated by a wide array of ligands on the site. The triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently described receptor that has many effects on human PMN. The engagement of TREM-1 on PMN can induce phagocytosis, reactive oxygen species production and release of myeloperoxidase and IL-8. LPS has a priming effect on these functions. We show in this paper that Lyn, AKT, extracellular signal-regulated kinase 1/2 and Jak2 signaling pathways are elicited following TREM-1 engagement and activation by a monoclonal agonist antibody (anti-TREM-1) in human PMN, leading to the phosphorylation of STAT5 and RelA, a subunit of the nuclear factor-kappa B family. We also show that TREM-1 is recruited to ganglioside M1-lipid rafts in PMN upon stimulation with LPS or anti-TREM-1. Moreover, we observed that Toll-like receptor 4 and TREM-1 co-localize upon stimulation and TREM-1 engagement resulted in the phosphorylation of IL-1R-associated kinase 1, but not its stimulant-induced degradation. These data shed a new light on how various receptors implicated in the innate immune response could interact to insure an efficient inflammatory response upon pathogens-associated aggression.
Keywords: inflammation, lipid rafts, PMN, TLR4, TREM-1
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