The figure indicates the percentage (%) of positive patients based on the detection limits of the tests. AAS = abdominal aortic surgery; …Plasma levels of cytokines, CRP, PCT, cortisol and leukocyte countsIn order to find more monitor the inflammatory process, IL-6, IL-10, CRP, PCT, and cortisol were assayed in plasma and leukocytes counted at various time points. As shown in Figure Figure5,5, significantly higher amounts of IL-6 and IL-10 were detected in the plasma of AAS patients as compared with CAS. IL-6 was detected in AAS plasma at T4 and the highest value was attained at POD1. The presence of IL-10 was maximal at T4 and high levels were maintained until POD2. In the CAS group, IL-10 and IL-6 levels were undetected in most cases. Plasma levels of CRP were measured at T1, T4, POD1, and POD2.

CRP levels started to increase at POD1 and were further increased at POD2 in both groups, but the increments were significantly higher in AAS patients than in CAS patients (Figure (Figure5).5). Similar patterns were also found in PCT levels, with the difference that the maximal value was reached at POD1 (Figure (Figure5).5). Similarly, there was a transient increase in leukocyte count at POD1 in AAS patients only, with values going back to normal at POD2 (data not shown). Plasma cortisol levels were not significantly different between AAS patients (111 �� 9 ng/ml) and CAS patients (105 �� 11 ng/ml) at T1. Both groups of patients showed a significant increase in plasma levels of cortisol at POD1 (AAS: 229 �� 44 ng/ml and CAS: 157 �� 26 ng/ml), with a tendency towards higher values for AAS patients (P = 0.

07).Figure 5Plasma levels of IL-10, IL-6, C-reactive protein and procalciton in in AAS and CAS patients. Plasma levels of cytokines, C-reactive protein (CRP), and procalcitonin (PCT) were measured at T1 (before anesthesia), T2 (before incision), T3 (before clamping), …Correlation between the levels of circulating NOD2 agonist and other parametersThe survey indicated that the inflammatory response took place after bacterial NOD2 agonist translocation. Among AAS patients, levels of circulating NOD2 agonist at T4 positively correlated with those of IL-10 at T4 and of cortisol at POD1 (r = 0.46, P = 0.04; and r = 0.55, P = 0.01, respectively). Interestingly, in AAS patients but not in CAS patients, cortisol levels at POD1 correlated with those of IL-10 at T4 and of PCT at POD1 (r = 0.59, P = 0.006; and r = 0.55, P = 0.02, respectively), Cilengitide and with the length of clamping (r = 0.45, P = 0.05). In AAS patients, the length of clamping correlated with levels of IL-6 at T4 and of PCT at POD1 (r = 0.53, P = 0.03; and r = 0.52, P = 0.02, respectively). There was no correlation between the length of clamping and levels of NOD2 agonist in the plasma.