Goat anti Human TREM1 polyclonal antibody [Biotin]

BACKGROUND: Cell and animal models show a key role for Triggering Receptor Expressed on Myeloid Cells (TREM)-2 in chronic airway disease after viral infection, but comparable evidence in humans still needs to be established. METHODS: Lung tissue samples were obtained from lung transplant recipients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage IV COPD (n = 16), nontransplantable donor lung tissues (n = 7), and resected lung tissues from patients at risk or with GOLD stage I through IV (n = 55) and were assessed for TREM-2 and TREM-1 messenger RNA (mRNA), protein expression, and other markers of a type 2 immune response. RESULTS: TREM2 (but not TREM1) mRNA levels were increased in GOLD stage IV COPD lung tissues compared with non-COPD lung tissues. TREM2 mRNA was coexpressed with its signaling molecule DAP12 and the macrophage marker CD68 and M2-macrophage markers CD206 and CHIT1. TREM-2 protein was also increased in COPD lung tissues and was localized to CD14(+) macrophages by flow cytometry and CD68(+) and CCR2(+) macrophages by tissue immunostaining. In lung samples from patients at risk and with GOLD stage I through IV COPD, TREM2 but not TREM1 mRNA levels were also increased, and the ratio of TREM2/TREM1 mRNA levels was associated with increases in CHIT1 mRNA and decreases in FEV1 and FEV1/FVC. CONCLUSIONS: TREM-2 expression is increased in lung macrophages in COPD, particularly in comparison with TREM-1. Therefore, TREM-2 levels and the ratio of TREM-2/TREM-1 signifies M2 activation in COPD lung tissues and may help to guide therapeutics directed against the type 2 immune response in patients with this disease.

Objective: To evaluate the accuracy of the soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) as a diagnostic test for bacterial infection. Design: Meta-analysis of 13 diagnostic studies. Data source: Medline; Embase; Web of Science (from January 1966 to January, update to August 2008); and Cochrane Controlled Clinical Trials Register Database (through first quarter 2008). Measurements and results: A meta-analysis of all 73 studies was performed. Thirteen studies fulfilled the inclusion criteria (980 patients, 557 patients with bacterial infection, 423 with nonbacterial infection); global prevalence was 56.8%. The global sensitivity was 0.82 (95% confidence interval CI, 0.68-0.90), the specificity was 0.86 (95% CI, 0.77-0.91), the positive likelihood ratio (PLR) was 5.66 (95% CI, 3.41-9.38), the negative likelihood ratio (NLR) was 0.21 (95% CI, 0.12-0.40), and the diagnostic odds ratio (DOR) was 26.35 (95% CI, 10.32-67.28). The area under the curve of the summary receiver operator characteristic (SROC) was 0.86 (95% CI, 0.77-0.91), with a Q point value of 0.84. The sensitivity of the sTREM-1 assay for diagnosis of urinary tract infection was low (0.18, 95% CI, 0.05-0.51). Conclusions: sTREM-1 represents a reliable biological marker of bacterial infection, but it may be not a sufficient biological marker for infection of the urinary tract as a result of its low sensitivity. Whether sTREM-1 guidance can reduce antibiotic use as well as the measurement of sTREM-1 in different types of infection will require additional prospective studies.