• Derek E Byers, Kangyun Wu, Geoffrey Dang-Vu, Xiaohua Jin, Eugene Agapov, Xiaofeng Zhang, John T Battaile, Kenneth Schechtman, Roger Yusen, Richard A Pierce, and Michael J Holtzman.
• Department of Medicine, Drug Discovery Program in Pulmonary and Critical Care, Washington University School of Medicine, Saint Louis, MO. Electronic address: dbyers@wustl.edu.
• Chest. 2018 Jan 1; 153 (1): 778677-86.

BackgroundCell 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.MethodsLung 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.ResultsTREM2 (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.ConclusionsTREM-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.Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

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