Respirology · 2007 · 33 citations · 16 references
Veterinary MedicineImmunologyPathologyImmunopathologyInflammationInnate ImmunityInflammation In Infectious DiseaseInflammatory BiomarkersInflammatory MediatorsPleural DiseasePleural MalignanciesPulmonary InflammationFlow Cytometry ImmunophenotypingInflammatory EffusionsMalignant Effusion DetectionMalignant Pleural EffusionPleural Effusion EvaluationPleural Effusion In MalignancyPleural InflammationTrem1 Signaling
BACKGROUND AND OBJECTIVE: The triggering receptor expressed on myeloid cell-1 (TREM-1) is a newly discovered molecule that is associated with the inflammatory response to microorganisms. We investigated the role of surface and soluble TREM-1 in differentiating different disease entities in pleural effusion formation. METHODS: Sixty-seven patients with pleural effusion due to transudate (14), malignancy (15), tuberculous pleuritis (16), para-pneumonic effusion (10) and empyaema (12) were included in this study. Surface TREM-1 was measured by flow cytometry and was expressed as mean fluorescence intensity and soluble TREM-1 was measured by ELISA and expressed as pg/mL. Results are given as mean levels +/- SEM. RESULTS: Surface TREM-1 was measured in 24 patients and the levels were highest in para-pneumonic effusion (30.0 +/- 8.4) and lowest in malignant pleural effusion (5.2 +/- 1.1) and tuberculous pleuritis (5.2 +/- 2.4). Soluble TREM-1 was highest in effusions of infectious aetiology (para-pneumonic effusion (979.4 +/- 229.6) and empyaema (1712.6 +/- 299.5)) and lowest in non-infectious effusions (transudate (81.2 +/- 4.5 pg/mL) and malignancy (111.3 +/- 20.7). At a cut-off value of 114 pg/mL, soluble TREM-1 yielded a sensitivity of 87.5% and a specificity of 89.7% in differentiating non-infectious effusion from tuberculous pleuritis. At a cut-off value of 374 pg/mL, sTREM-1 yielded a sensitivity of 93.8% and a specificity of 90.9 in differentiating tuberculous pleuritis from bacterial pleural effusion. CONCLUSION: Soluble and surface TREM-1 are valuable markers in establishing the aetiology of pleural effusions.
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TREM-1 amplifies inflammation and is a crucial mediator of septic shock
Axel Bouchon, Fabio Facchetti, Markus A. Weigand et al. · Nature · 2001 · 1.1K citations
Sébastien Gibot, Marie‐Nathalie Kolopp‐Sarda, Marie C. Béné et al. · Annals of Internal Medicine · 2004 · 407 citations