Hemofiltration reduces the serum priming activity on neutrophil chemiluminescence in septic patients

Background. Priming of the polymorphonuclear neutrophil (PMN) response has been implicated in the activation of oxidative burst and tissue injury in p atients with septic shock and acute renal failure (ARF). This study evaluat ed whether hemofiltration (HF) removes substances able to enhance the oxida tive burst of PMNs. Methods. Chemiluminescence (CL) priming activity induced by sera and ultraf iltrates of seven patients with septic shock, multiorgan dysfunction syndro me, and ARF (ARF/HF group) and of 10 uremic stable patients (Control/HF gro up) was evaluated on normal human PMNs stimulated with bacterial formylmeth ionyl-teucyl-phenytalanine (FMLP). Patients submitted to HF were studied by determining blood and ultrafiltrate interleukin-8 (IL-8), platelet-activat ing factor (PAF), and CL priming activity at the beginning (T-0), and after four hours (T-4) of treatment. Results. Preincubation of normal human PMNs with sera and ultrafiltrates fr om septic patients induced a potent priming of CL activity in subsequent FM LP stimulation. In the ARF/HF group, the prefilter blood concentrations of IL-8 and CL PMN-priming activity significantly decreased during the four ho urs of HF treatment, with a loss of IL-8 in the ultrafiltrate of 6930 (medi an. range 4292 to 9282) ng per four hours. PAF detected in the ultrafiltrat e and associated with the membrane (7.3 ng, range 1.45 to 9.89) was minimal . In the ARF/HF group, a significantly positive correlation between CL PMN- priming activity and IL-8 concentrations was observed. The CL priming activ ity in blood and ultrafiltrates was reduced to 55 and 46% by preabsorption with monoclonal antibody (mAb) anti-IL-8. In contrast, the PAF receptor ant agonist WEB 2170 did not affect CL priming activity. In the control/HF grou p, the CL PMN-priming activity was significantly lower than in the ARF/HF g roup and was independent of IL-8. Conclusions. Sera from septic patients demonstrate an enhanced CL priming a ctivity on PMNs. This activity is reduced by ultrafiltration and is due, at least in part, to ultrafiltered IL-8.