E of cytokines and chemokines, prostaglandins and matrixdegrading enzymes. These substances trigger uterine contractions, membrane rupture and cervical ripening [4]. Evidence suggeststhat most intra-uterine infections are chronic and subclinical in nature and consequently hard to diagnose before labor or rupture of membranes [1,4,5]. Therefore a diagnostic marker of subclinical infection or inflammation would be most useful to identify women at risk for PTB. Recently, a family of cell surface receptors, the triggering receptor expressed on myeloid cells (TREM) proteins, has been discovered that seems to play an important role in fine-tuning the innate immune response during infectious diseases. Benzocaine TREM-1 is a transmembrane glycoprotein, mainly expressed in monocytes and neutrophils [8?4]. Studies have shown that TREM-1 expressionSerum sTREM-1 in Laboris upregulated in response to lipopolysaccharide (LPS) and other microbial components [8?4]. TREM-1 synergizes with pathogen recognition 
receptors, including Toll-like receptors (TLRs), which in turn, increase cytokine production (e.g. IL-8, TNF-a and IL1a)[8?4]. Hence, TREM-1 functions as an amplifier of the inflammatory response in the context of bacterial infection [8?4]. During infection, soluble TREM-1 (sTREM-1) is generated through proteolytic cleavage of the TREM-1 ectodomain by matrix metalloproteinases [10,14]. sTREM-1 is detectable in various body fluids [10,12] and has been detected in plasma, broncho-alveolar lavage fluid, pleural fluid, cerebrospinal fluid and urine from intensive care patients with bacterial infections [12]. Recent studies have demonstrated that TREM-1 is also involved in non-infectious inflammatory conditions such as rheumatoid arthritis [15] and inflammatory bowel disease [16]. Few studies have investigated the role of sTREM-1 during PTB [6,17?9]. Menon et al [18] demonstrated that both lipopolysaccharide (LPS) and preterm labor induced fetal membrane TREM1 expression. In the presence of intra-uterine infection, amniotic fluid sTREM-1 concentrations were significantly higher in patients with preterm labour (PTL) [6,18] or preterm premature rupture of the membranes (PPROM) [6]. However, amniotic fluid LY-2409021 price TREMlevels did not predict PTB within 7 days in women with PPROM [20]. Elevated serum concentrations of sTREM-1 in the second trimester were associated with an increased risk of PTB in asymptomatic high risk patients [19], but not in low-risk women [17]. Furthermore, it has been shown that amniotic fluid concentration of sTREM-1 increases with advancing gestational age [6]. To our knowledge, only two studies [21,22] evaluated serum sTREM-1 concentrations in patients with preterm labor. Blood sampling has the advantage of being less invasive than amniocentesis and is therefore a more appropriate method to perform in pregnancy. However, these studies did not include women with term labor. There is accumulating evidence that inflammation has also been implicated in the mechanism of spontaneous term parturition [2,7]. Youssef et al [23] demonstrated that TREM-1 1317923 is expressed in myometrium and cervix at term and found that sTREM-1 is upregulated in both tissues with the onset of labor. Therefore, the objective of the present study was to evaluate whether sTREM-1 is upregulated in maternal serum during term and preterm labor vs. non laboring controls and to assess a possible relationship between sTREM-1 serum concentrations and admission-to-delivery interval in women with.E of cytokines and chemokines, prostaglandins and matrixdegrading enzymes. These substances trigger uterine contractions, membrane rupture and cervical ripening [4]. Evidence suggeststhat most intra-uterine infections are chronic and subclinical in nature and consequently hard to diagnose before labor or rupture of membranes [1,4,5]. Therefore a diagnostic marker of subclinical infection or inflammation would be most useful to identify women at risk for PTB. Recently, a family of cell surface receptors, the triggering receptor expressed on myeloid cells (TREM) proteins, has been discovered that seems to play an important role in fine-tuning the innate immune response during infectious diseases. TREM-1 is a transmembrane glycoprotein, mainly expressed in monocytes and neutrophils [8?4]. Studies have shown that TREM-1 expressionSerum sTREM-1 in Laboris upregulated in response to lipopolysaccharide (LPS) and other microbial components [8?4]. TREM-1 synergizes with pathogen recognition receptors, including Toll-like receptors (TLRs), which in turn, increase cytokine production (e.g. IL-8, TNF-a and IL1a)[8?4]. Hence, TREM-1 functions as an amplifier of the inflammatory response in the context of bacterial infection [8?4]. During infection, soluble TREM-1 (sTREM-1) is generated through proteolytic cleavage of the TREM-1 ectodomain by matrix metalloproteinases [10,14]. sTREM-1 is detectable in various body fluids [10,12] and has been detected in plasma, broncho-alveolar lavage fluid, pleural fluid, cerebrospinal fluid and urine from intensive care patients with bacterial infections [12]. Recent studies have demonstrated that TREM-1 is also involved in non-infectious inflammatory conditions such as rheumatoid arthritis [15] and inflammatory bowel disease [16]. Few studies have investigated the role of sTREM-1 during PTB [6,17?9]. Menon et al 
[18] demonstrated that both lipopolysaccharide (LPS) and preterm labor induced fetal membrane TREM1 expression. In the presence of intra-uterine infection, amniotic fluid sTREM-1 concentrations were significantly higher in patients with preterm labour (PTL) [6,18] or preterm premature rupture of the membranes (PPROM) [6]. However, amniotic fluid TREMlevels did not predict PTB within 7 days in women with PPROM [20]. Elevated serum concentrations of sTREM-1 in the second trimester were associated with an increased risk of PTB in asymptomatic high risk patients [19], but not in low-risk women [17]. Furthermore, it has been shown that amniotic fluid concentration of sTREM-1 increases with advancing gestational age [6]. To our knowledge, only two studies [21,22] evaluated serum sTREM-1 concentrations in patients with preterm labor. Blood sampling has the advantage of being less invasive than amniocentesis and is therefore a more appropriate method to perform in pregnancy. However, these studies did not include women with term labor. There is accumulating evidence that inflammation has also been implicated in the mechanism of spontaneous term parturition [2,7]. Youssef et al [23] demonstrated that TREM-1 1317923 is expressed in myometrium and cervix at term and found that sTREM-1 is upregulated in both tissues with the onset of labor. Therefore, the objective of the present study was to evaluate whether sTREM-1 is upregulated in maternal serum during term and preterm labor vs. non laboring controls and to assess a possible relationship between sTREM-1 serum concentrations and admission-to-delivery interval in women with.