Fiche publication
Date publication
août 2005
Auteurs
Membres identifiés du Cancéropôle Est :
Pr FAURE Gilbert
Tous les auteurs :
Gibot S, Massin F, Le Renard P, Bene MC, Faure GC, Bollaert PE, Levy B
Lien Pubmed
Résumé
OBJECTIVE: To examine the expression patterns of the triggering receptor expressed on myeloid cells (TREM)-1 during experimental septic shock. DESIGN: Animal study. SETTING: Animal research laboratory. SUBJECTS: Male BALB/c mice, 7-9 wks of age. INTERVENTIONS: Septic shock was induced by cecal ligation and puncture in eight mice. Eight additional animals were sham-operated and served as a control group. All animals were resuscitated by fluid infusion and administered antibiotics. Kill was performed under anesthesia 12, 24, or 48 hrs later. MEASUREMENTS AND MAIN RESULTS: Surface expression of TREM-1 was analyzed using flow cytometry on peripheral blood cells, peritoneal macrophages and neutrophils, splenic macrophages, and Kupffer cells. Gene expression was also studied in these same cells using reverse transcription-polymerase chain reaction. Tumor necrosis factor-alpha, interleukin-1beta, and soluble TREM-1 concentrations were determined in plasma and peritoneal lavage fluid. Sepsis strongly induced TREM-1 gene expression, which translated into an up-regulation of TREM-1 surface expression on neutrophils and monocytes/macrophages both at the focus on infection as well as distally. Moreover, sepsis induced the release of significant levels of soluble TREM-1. Plasma soluble TREM-1 concentrations negatively correlated with tumor necrosis factor-alpha and interleukin-1beta levels at 12 hrs. CONCLUSIONS: These results provide new information as to the regulation of TREM-1 during sepsis. Considering that both cell-surface and soluble TREM-1 were strongly up-regulated during infection, this study may add support to the putative usefulness of TREM-1 as a diagnostic tool.
Référence
Crit Care Med. 2005 Aug;33(8):1787-93.
