Monocytes in systematic inflammatory response syndrome: differences between sepsis and acute pancreatitis
Abstract number: p1178
Baziaka F., Tsaganos T., Kousoulas V., Karagianni V., Pelekanou A., Antonopoulou A., Giamarellos-Bourboulis E.J.
Monocytes release pro-inflammatory cytokines leading to inflammatory response syndrome (SIRS). The present study aimed to unravel the differences of monocyte triggering between SIRS of patients with acute pancreatitis compared to SIRS of patients with sepsis.
Peripheral blood monocytes were isolated from 25 patients by density gradient centrifugation of whole blood, incubation in RPMI and removal of non-adherent cells. Twelve patients had sepsis and 13 patients acute pancreatitis; in all symptoms presented within 12 hours before admission. After diagnosis 20 ml blood was sampled. Half were assayed for isolation of monocytes and 10 ml were centrifuged for serum estimation of tumour necrosis alpha (TNF-a) and interleukin-6 (IL-6). Half of monocytes were incubated in the presence of 4% of patients' serum and supernatants were collected. The other half was lyzed; caspase-3 was estimate in the lysate by an enzymatic chromogenic assay. TNF-a and IL-6 were estimated in serum and cell supernatants by an enzyme immunoassay.
Median ± SE of TNF-a of serum in septic patients and in patients with acute pancreatitis was 11.61 ± 7.57 and 17.01 ± 8.64 pg/ml, respectively. Respective values of IL-6 in septic patients and those with acute pancreatitis were 192.30 ± 35.40 and 21.00 ± 16.05 pg/ml (p = 0.001). Respective values of intracellular activity of caspase-3 were 0.94 ± 0.17 and 0.34 ± 0.09 pmol/min.104 cells, (p = 0.049). TNF-a of monocyte supernatants did not differ between patients with acute pancreatitis and sepsis, a result that remain unaltered in the presence of patients' serum. IL-6 of monocyte supernatants of patients with sepsis was considerably increased after addition of patients' serum compared to patients with pancreatitis (see Figure).
The data have shown that monocyte activity was different between acute pancreatitis and sepsis. The different kinetics of the release of IL-6 might speculate for the existence of a probable anti-inflammatory mechanism active in acute pancreatitis but not in sepsis.
|Session name:||XXIst ISTH Congress|
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