OBJECTIVE: To investigate the activating properties of serum from septic patients on monocytes and the potential effect of plasmapheresis. DESIGN: Prospective controlled study. SETTING: Teaching hospital, Germany. SUBJECTS: 7 Patients with life-threatening systemic inflammatory response syndrome (SIRS) and 4 control patients with serious but not life-threatening conditions. INTERVENTIONS: We measured the amount of mediators released by healthy donor monocytes incubated in serum and separated plasma from septic patients. MAIN OUTCOME MEASURES: Release of interleukin 6 (IL-6), prostaglandin E2 (PGE2), interleukin 1 (IL-1), and tumour necrosis factor (TNF). RESULTS: The serum and separated plasma from infected patients selectively induced the release of IL-6 and PGE2. The mean PGE2 production in serum was 10,895 pg/ml/10(5) cells, and in plasma was 14,023 pg/ml/10(5) cells compared with a control of 0 (p < 0.05). The mean IL-6 production in serum was 4925 pg/ml/10(5) cells and in plasma 4262 pg/ml/10(5) cells compared with a control of 0 (p < 0.05). In contrast, IL-1 and TNF did not seem to be associated with sepsis and were present in small amounts if at all. Additional stimulation with lipopolysaccharide (LPS) increased the serum and plasma induced release of PGE2 and IL-6 (p < 0.05). Serum and plasma from septic patients did, however, selectively reduce the maximum LPS-stimulated release of PGE2 and TNF (p < 0.05) compared with healthy donor monocytes. CONCLUSION: Serum and separated plasma from septic patients contained agents which induced monocytes to release mediators without additional stimulation, and modified their response to LPS. Removing plasma from septic patients may therefore reduce the deleterious effect of the inflammatory response.
OBJECTIVE: To investigate the activating properties of serum from septic patients on monocytes and the potential effect of plasmapheresis. DESIGN: Prospective controlled study. SETTING: Teaching hospital, Germany. SUBJECTS: 7 Patients with life-threatening systemic inflammatory response syndrome (SIRS) and 4 control patients with serious but not life-threatening conditions. INTERVENTIONS: We measured the amount of mediators released by healthy donor monocytes incubated in serum and separated plasma from septic patients. MAIN OUTCOME MEASURES: Release of interleukin 6 (IL-6), prostaglandin E2 (PGE2), interleukin 1 (IL-1), and tumour necrosis factor (TNF). RESULTS: The serum and separated plasma from infected patients selectively induced the release of IL-6 and PGE2. The mean PGE2 production in serum was 10,895 pg/ml/10(5) cells, and in plasma was 14,023 pg/ml/10(5) cells compared with a control of 0 (p < 0.05). The mean IL-6 production in serum was 4925 pg/ml/10(5) cells and in plasma 4262 pg/ml/10(5) cells compared with a control of 0 (p < 0.05). In contrast, IL-1 and TNF did not seem to be associated with sepsis and were present in small amounts if at all. Additional stimulation with lipopolysaccharide (LPS) increased the serum and plasma induced release of PGE2 and IL-6 (p < 0.05). Serum and plasma from septic patients did, however, selectively reduce the maximum LPS-stimulated release of PGE2 and TNF (p < 0.05) compared with healthy donor monocytes. CONCLUSION: Serum and separated plasma from septic patients contained agents which induced monocytes to release mediators without additional stimulation, and modified their response to LPS. Removing plasma from septic patients may therefore reduce the deleterious effect of the inflammatory response.