• Tuberculosis and Respiratory Diseases
• /
• v.62 no.6
• /
• pp.499-505
• /
• 2007

Background: Triggering receptor expressed on myeloid cells 1 protein (TREM-1) is a cell surface molecule expressed on neutrophils and monocytes, and it plays an important role in myeloid cell-activated inflammatory response. The aim of this study was to investigate the diagnostic efficiency of soluble (s) TREM-1 in the patients who had pleural effusion from various causes. Methods: Forty-five patients with exudative pleural effusion were included in this study. The level of sTREM-1 was measured in both the serum and pleural fluids by immunoblot assay with using human-sTREM-1 antibody. Results: The pleural fluid sTREM-1 was significantly different in the three groups of exudative pleural effusion (p=0.011). Particularly, the patients with parapneumonic effusion were found to have significantly higher pleural fluid levels of sTREM-1 than patients with tuberculous (p<0.05) and malignant effusion, respectively (p<0.05). However, the serum sTREM-1 did not show a significant difference in the three groups. In order to evaluate the diagnostic utility of pleural fluid sTREM-1, the receiver operating characteristic (ROC) curve was constructed and the area under the curve (AUC) was 0.818 (p=0.001). Using a cutoff value of 103.5 pg/mL for the pleural fluid sTREM-1, the sensitivity and specificity were 73% and 81%, respectively, for differentiating parapneumonic effusion from tuberculous or malignant effusions. Conclusion: Pleural fluid sTREM-1 can be an additional marker for making the differential diagnosis of pleural effusion.

• Tuberculosis and Respiratory Diseases
• /
• v.62 no.4
• /
• pp.290-298
• /
• 2007

Background: The currently available diagnostic markers for pleural effusion have a limited role. The soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is a molecule recently reported to play an important role in the myeloid cell mediated inflammatory response, and is up regulated in the body fluid by bacterial or fungal products. This study examined the expression of sTREM-1 in pleural effusion. Methods: Between April 2004 and December 2005, 48 patients with pleural effusions were enrolled in this study. The pleural fluids were taken and analyzed for the total protein, glucose, lactate dehydrogenase (LDH), adenosine deaminase (ADA), and sTREM-1. Bacterial cultures and cytology tests were also performed. Results: The clinical diagnoses were 17 parapneumonic, 14 tuberculous, and 13 malignant effusions. Four patients presented with transudates. The mean ages of the parapneumonic, tuberculous and malignant effusion groups were $57.1{\pm}19.7$, $49.5{\pm}18.6$, $66.9{\pm}15.5$, and $76.0{\pm}18.1$. respectively. The level of sTREM-1 expression was significantly higher in the parapneumonic effusions ($344.0{\pm}488.7$) than in the tuberculous effusions ($81.7{\pm}56.6$) and malignant effusions ($39.3{\pm}19.6$). With a cut-off value of 55.4pg/ml, the sensitivity and specificity for a parapneumonic effusion was 70.6% and 74.1%. Conclusion: sTREM-1 expression is significantly higher in parapneumonic effusions, suggesting its potential role as an additional diagnostic marker for pleural effusions.

• Tuberculosis and Respiratory Diseases
• /
• v.65 no.4
• /
• pp.301-307
• /
• 2008

Background: The triggering receptor expressed on myeloid cells-1 (TREM-1) is an activating receptor that is expressed on the surface of neutrophils and mature monocytes when stimulated with several microbial components, which can amplify the inflammatory response. This study analyzed the prognostic value of the sTREM-1 levels in patients with acute respiratory distress syndrome (ARDS). Methods: The bronchoalveolar lavage (BAL) fluid and blood was collected prospectively from 32 patients with ARDS, 15 survivors and 17 nonsurvivors. An enzyme-linked immunosorbent assay was performed to measure the sTREM-1. The following data was obtained: APACHE II score, Clinical Pulmonary Infection Score (CPIS), BAL fluid analysis, C-reative protein. Mortality in the ICU was defined as the end point. Results: The serum sTREM-1 level was significantly higher in the nonsurvivors than survivors ($54.3{\pm}10.3pg/ml$ vs. $22.7{\pm}2.3pg/ml$, p<0.05). The sTREM-1 level in the serum, but not in the BAL fluid, was an independent predictor of the ICU mortality (OR: 22.051, 95% CI: 1.780~273.148, p<0.016), and a cut-off value of ${\geq}33pg/ml$ yielded a diagnostic sensitivity of 71% and specificity of 93%. Conclusion: The serum sTREM-1 level may be a useful predictor of the outcome of ARDS patients.

• IMMUNE NETWORK
• /
• v.24 no.2
• /
• pp.3.1-3.23
• /
• 2024

Cigarette smoke extract (CSE)-treated mouse airway epithelial cells (MAECs)-derived exosomes accelerate the progression of chronic obstructive pulmonary disease (COPD) by upregulating triggering receptor expressed on myeloid cells 1 (TREM-1); however, the specific mechanism remains unclear. We aimed to explore the potential mechanisms of CSE-treated MAECs-derived exosomes on M1 macrophage polarization and pyroptosis in COPD. In vitro, exosomes were extracted from CSE-treated MAECs, followed by co-culture with macrophages. In vivo, mice exposed to cigarette smoke (CS) to induce COPD, followed by injection or/and intranasal instillation with oe-TREM-1 lentivirus. Lung function and pathological changes were evaluated. CD68⁺ cell number and the levels of iNOS, TNF-α, IL-1β (M1 macrophage marker), and pyroptosis-related proteins (NOD-like receptor family pyrin domain containing 3, apoptosis-associated speck-like protein containing a caspase-1 recruitment domain, caspase-1, cleaved-caspase-1, gasdermin D [GSDMD], and GSDMD-N) were examined. The expression of maternally expressed gene 3 (MEG3), spleen focus forming virus proviral integration oncogene (SPI1), methyltransferase 3 (METTL3), and TREM-1 was detected and the binding relationships among them were verified. MEG3 increased N6-methyladenosine methylation of TREM-1 by recruiting SPI1 to activate METTL3. Overexpression of TREM-1 or METTL3 negated the alleviative effects of MEG3 inhibition on M1 polarization and pyroptosis. In mice exposed to CS, EXO^-CSE further aggravated lung injury, M1 polarization, and pyroptosis, which were reversed by MEG3 inhibition. TREM-1 overexpression negated the palliative effects of MEG3 inhibition on COPD mouse lung injury. Collectively, CSE-treated MAECs-derived exosomal long non-coding RNA MEG3 may expedite M1 macrophage polarization and pyroptosis in COPD via the SPI1/METTL3/TREM-1 axis.