Triggering receptor expressed on myeloid cells (TREM)-1 is a recently described receptor on neutrophils and monocytes. It behaves like a pattern recognition receptor (PRR) since its activation leads to the release of pro-inflammatory cytokines, namely of tumour necrosis factor-alpha (TNFα) and of interleukin (IL)-8. Although its ligand is still unknown, activation is mediated by bacteria and fungi [3, 4] . A soluble form of TREM-1, namely sTREM-1, is increased in the bronchoalveolar lavage (BAL) of patients with ventilator associated pneumonia (VAP) [5, 6] , and in the serum of patients with sepsis, with bacterial meningitis and with acute pancreatitis [7] [8] [9] [10] [11] [12] . This same soluble form of TREM-1 seems to be increased in patients bearing noninfectious processes like peptic ulcer, inflammatory bowel disease, viral infections, malignant pleural effusions and chronic obstructive pulmonary disease (COPD) but also among patients after cardiac surgery or cardiac arrest. Increase of sTREM-1 seems particular prominent when the latter non-infectious states are complicated with systemic inflammatory response syndrome (SIRS) without infection [13] [14] [15] [16] [17] [18] [19] .