4a). IL-6 concentration was higher in non-survivors than in healthy volunteers three days after admission (Figure (Figure3b),3b), but no difference was observed in IL-10 concentrations at this point (Figure (Figure4b).4b). Both cytokines were increased at admission in uninfected patients but declined three days later (Figures (Figures3c3c and and4c).4c). In contrast, selleck chemicals 17-AAG in infected patients, IL-6 and IL-10 concentrations were higher than in healthy volunteers at admission and three days later (Figures (Figures3c3c and and4c4c).Figure 3IL-6 concentration was higher in patients with severe AP and in infected patients. IL-6 concentration was measured in serum from patients with mild acute pancreatitis (AP; n = 18), patients with severe AP (n = 11), and healthy volunteers (n = 36). Samples …
Figure 4IL-10 concentration was higher in patients with severe AP and in infected patients. IL-10 concentration was measured in serum from patients with mild acute pancreatitis (AP; n = 18), patients with severe AP (n = 11), and healthy volunteers (n = 19). …DiscussionOne of the most serious complications of AP is the development of infection. The aim of this study was to measure the levels of TREM-1 and HLA-DR on monocytes and the serum concentrations of IL-6 and IL-10 in patients with AP to determine whether these markers, alone or in combination, can be used in the early identification of patients at high risk of developing severe AP or infection. Our results suggest that TREM-1 expression increases in the presence of inflammation because it was higher in all patients with AP, regardless of the presence of infection.
These results support our previous study showing that TREM-1 expression increases after surgery, particularly in patients with preexisting SIRS, but does not correlate with the presence of infection [19]. TREM-1 may be involved in the amplification of the inflammatory response in AP, and its ligand could be an endogenous molecule released during cellular damage associated with AP [24]. Wang and colleagues found higher levels of TREM-1 mRNA in patients with severe AP than in patients with mild AP and healthy volunteers [20]. This seems in contrast to our results, but we measured protein levels and not mRNA, and mRNA levels do not necessarily correlate with protein levels.
TREM-1 can be shed from the surface of monocytes by matrix metalloproteinases [25], and these enzymes are increased in serum in animal models of severe AP [26,27] and in patients with severe AP [28,29]. We found higher TREM-1 expression on monocytes Drug_discovery from patients with AP, compared with monocytes from healthy volunteers, but the levels did not differ between patients with mild and severe AP. Perhaps the metalloproteinases found in the serum of patients with severe AP prevented a further increase on TREM-1 expression, but we did not find differences in the concentrations of soluble TREM-1 in serum between patients with mild and severe AP.