Plasma Neutrophil Elastase Research Articles

Neutrophil CD64 expression is associated with severity and prognosis of disseminated intravascular coagulation

Introduction Although neutrophil can be activated by microcirculatory disturbances in DIC, its relation with the severity and prognosis of DIC has not been elucidated. We investigated the relationship between neutrophil activation and DIC severity and determined the prognostic value of neutrophil activation markers in patients with DIC. Materials and methods We measured two neutrophil activation markers, neutrophil CD64 expression and plasma neutrophil elastase, in 94 patients with suspected DIC and 55 healthy controls. Neutrophil CD64 expression and plasma neutrophil elastase were measured using CD64 quantitation kit, and PMN Elastase enzyme immunoassay kit. Results Neutrophil CD64 expression and plasma neutrophil elastase level were significantly increased in patients with overt and non-overt DIC compared to normal controls ( P < 0.001, each). Neutrophil CD64 expression showed a significant linear trend of increase with increasing DIC score ( P < 0.001). In DIC patients, significant differences were observed between those with and without infection both in overt ( P = 0.003) and non-overt DIC ( P = 0.004). Neutrophil CD64 expression was significantly increased in 28-day non-survival group compared to survival group in both overt ( P < 0.001) and non-overt DIC ( P = 0.032). The 28-day survival rate showed a stronger association with the neutrophil CD64 expression ( P < 0.001) than with DIC score ( P = 0.028) or plasma neutrophil elastase level ( P = 0.246). Conclusions Neutrophil CD64 expression is significantly correlated with DIC severity and has a good predictive value for the 28-day mortality in patients suspected of having DIC. Neutrophil CD64 expression might be useful in monitoring the disease course and in predicting mortality in DIC patients.

Association of plasma neutrophil elastase levels with other inflammatory mediators and clinical features in adult patients with moderate and severe pneumonia

Plasma levels of neutrophil elastase (NE) are elevated in several inflammatory diseases and thus this enzyme might be a critical inflammatory marker. However, the role of NE in the pathogenesis of pneumonia has not been determined. The association between the severity of pneumonia and blood levels of inflammatory markers could be relevant to developing a useful indicator of severity and new therapeutic strategies for pneumonia. We searched for a useful predictive marker and a new therapeutic strategy against pneumonia, using a prospective, multicenter, population-based investigation. Several inflammatory markers in the circulation including NE, cytokines, defensins, C-reactive protein (CRP) and white blood cell (WBC) counts as well as clinical features were prospectively monitored in 28 adult patients with moderate (n=11) and severe pneumonia (n=17) over a period of 14 days. The value of plasma NE was the highest at entry and significantly declined 2 days later. Trends of cytokines, defensins, CRP and WBC counts were similar but blunter. Microorganisms and the outcome of initial treatment did not significantly affect plasma NE levels. Baseline values of plasma NE were significantly higher in severe, than in moderate pneumonia and this difference between the two types of pneumonia persisted longer than those of any other markers. Neutrophil elastase appears to play a critical role in severe pneumonia and determination of its concentration in blood could be a useful indicator of severity. Furthermore, clinical trials of anti-NE drugs in patients with severe pneumonia should be promising.

Neutrophil Elastase as a Predicting Factor for Development of Acute Lung Injury

To determine whether the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) associated with systemic inflammatory response syndrome (SIRS) can be predicted by the plasma neutrophil elastase level. Patients were sequentially enrolled after obtaining informed consent. Twenty-three adult patients with SIRS were classified into the following groups; SIRS alone (5 patients), Group A of ALI/ARDS with SIRS (9 patients) that did not require mechanical ventilation, and Group B of ALI/ARDS with SIRS (9 patients) that required mechanical ventilation. Blood samples were obtained after the diagnosis of SIRS, and the sequential sampling was performed. The plasma neutrophil elastase level was significantly elevated in all patient groups as compared with healthy controls (43.7+/-5.4 ng/ml). The elastase levels in SIRS alone, Group A of ALI/ARDS, and Group B of ALI/ARDS were 126.9+/-11.0 ng/ml, 316.2+/-68.9 ng/ml, and 458.4+/-132.8 ng/ml, respectively. The elastase level in ALI/ARDS with SIRS was significantly greater than that in SIRS alone. The maximal level in 13 of 18 patients with ALI/ARDS with SIRS was more than 220 ng/ml. The level in all patients with SIRS alone was consistently less than 220 ng/ml over the study period. The serum levels of inflammatory cytokines were elevated in these patients, but no statistical significance was detected among the groups. The critical level of plasma neutrophil elastase is 220 ng/ml, and the SIRS patients with more than 220 ng/ml neutrophil elastase are highly likely to develop ALI/ARDS.

MMP-1 activation by serine proteases and MMP-10 induces human capillary tubular network collapse and regression in 3D collagen matrices

Previous work has shown that endothelial cell (EC)-derived matrix metalloproteinases (MMPs) regulate regression of capillary tubes in vitro in a plasmin- and MMP-1 dependent manner. Here we report that a number of serine proteases can activate MMP-1 and cause capillary tube regression; namely plasma kallikrein, trypsin, neutrophil elastase, cathepsin G, tryptase and chymase. Plasma prekallikrein failed to induce regression without coactivators such as high molecular weight kininogen (HMWK) or coagulation Factor XII. The addition of trypsin, the neutrophil serine proteases (neutrophil elastase and cathepsin G) and the mast cell serine proteases (tryptase and chymase) each caused MMP-1 activation and collagen type I proteolysis, capillary tubular network collapse, regression and EC apoptosis. Capillary tube collapse is accompanied by collagen gel contraction, which is strongly related to the wound contraction that occurs during regression of granulation tissue in vivo. We also report that proMMP-10 protein expression is markedly induced in ECs undergoing capillary tube morphogenesis. Addition of each of the serine proteases described above led to activation of proMMP-10, which also correlated with MMP-1 activation and capillary tube regression. Treatment of ECs with MMP-1 or MMP-10 siRNA markedly delayed capillary tube regression, whereas gelatinase A (MMP-2), gelatinase B (MMP-9) and stromelysin-1 (MMP-3) siRNA-treated cells behaved in a similar manner to controls and regressed normally. Increased expression of MMP-1 or MMP-10 in ECs using recombinant adenoviral delivery markedly accelerated serine protease-induced capillary tube regression. ECs expressing increased levels of MMP-10 activated MMP-1 to a greater degree than control ECs. Thus, MMP-10-induced activation of MMP-1 correlated with tube regression and gel contraction. In summary, our work demonstrates that MMP-1 zymogen activation is mediated by multiple serine proteases and MMP-10, and that these events are central to EC-mediated collagen degradation and capillary tube regression in 3D collagen matrices.

SIVELESTAT, A NEUTROPHIL ELASTASE INHIBITOR, ATTENUATES NEUTROPHIL PRIMING AFTER HEPATOENTERIC ISCHEMIA IN RABBITS

Neutrophils play an important role in ischemia-reperfusion injury. The neutrophil elastase not only causes tissue damage, but also mediates neutrophil priming. In the present study, we use a rabbit model of hepatoenteric ischemia-reperfusion to test the hypothesis that neutrophil elastase inhibition ameliorates an ischemia-reperfusion injury by attenuating neutrophil priming and suppressing enzymatic activity. Twenty-four Japanese white rabbits underwent 30 min of supraceliac aortic cross-clamping and 180 min of reperfusion under isoflurane anesthesia. The rabbits randomly received the neutrophil elastase inhibitor, sivelestat (n = 10), or saline (n = 14). Neutrophil priming was then assayed with luminol-dependent neutrophil chemiluminescence. Hepatic, intestinal, renal, and pulmonary damages were assessed with serum transaminase, lactate dehydrogenase concentrations, urinary N-acetyl glucosaminidase activity, and protein concentration in post mortem bronchoalveolar lavage fluid. We discovered that neutrophil elastase inhibition suppressed plasma neutrophil elastase, and that lipid peroxide concentrations increased after reperfusion. It improved ischemia-reperfusion injuries in the liver, intestine, kidney, and lung. Furthermore, inhibition of neutrophil elastase with sivelestat significantly attenuated post-reperfusion neutrophil priming. The results of this study demonstrate that neutrophil elastase inhibition could effectively attenuate an ischemia-reperfusion injury caused by supraceliac aortic cross-clamping, most likely from the attenuation of neutrophil priming.

Changes in Plasma Level of Human Leukocyte Elastase During Leukocytosis from Physical Effort

Physical exercise is known to induce immunological changes, mainly leukocytosis and neutrophil activation. However, it is not known to what extent the leukocytosis, observed after exertion, is associated with an increase in plasma neutrophil elastase, an early marker of inflammatory response and neutrophil degranulation. In the present study changes in circulating leukocyte and neutrophil counts and human neutrophil elastase plasma levels were evaluated in volley‐ball players before and after 2 h and 12 h prolonged training, during a competition season. For comparison, the same parameters were evaluated in untrained subjects before and after a jogging session. Basal white blood cell WBC, polymorpho nuclear PMN, and human polymorpho nuclear‐elastase PMN‐ELA values were within the normal healthy reference range and no significant differences were found between the two groups studied. Venous blood samples of nine volley‐ball players showed a statistically significant increase in blood WBCs after 2 h exercise. This effect was paralleled by a statistically significant increase in PMN‐ELA concentration compared to the values observed in the same individuals at rest. The exercise did not significantly change the basal correlation parameters between PMN level and PMN‐ELA concentration. More pronounced WBC, PMN, and PMN‐ELA increases were observed in the seven inactive subjects after 2 h jogging. There was no linear correlation between increased PMN counts and increased PMN‐ELA concentrations in untrained subjects after exercise. The results show that not only the leukocyte count but also PMN‐ELA plasma levels can be higher after physical effort. This has a practical significance as regards differential diagnosis demonstrating that determination of these two laboratory parameters can give abnormally high values even in the absence of an existing inflammatory process. Besides, lack of correlation between PMN count and PMN‐ELA plasma levels in the untrained group suggest a state in which activation of the neutrophils is not connected with their number in peripheral blood.

Inhibition of neutrophil elastase activity attenuates complement-mediated lung injury in the hamster

The role of neutrophil elastase in complement-mediated lung injury was examined in hamsters using a specific neutrophil elastase inhibitor, sodium N-[2-[4-(2,2 dimethylpropionyloxy)phenylsulfonylamino]benzoyl]aminoacetate tetrahydrate (sivelestat). Intravenous injection with cobra venom factor (CVF) into hamsters transiently increased plasma neutrophil elastase activity by about 10-fold. This increase was followed by a sustained increase in lung vascular [ 125I]bovine serum albumin permeability peaking 30 min after CVF injection. The increase in lung vascular permeability was associated with neutrophil accumulation in lung tissue and an increase in protein concentration in the bronchoalveolar lavage fluid. Inhibition of the elevated plasma neutrophil elastase activity (36.5%, 66.9% and 104.3%) by continuous i.v. infusion with sivelestat (0.1, 0.3 and 1 mg/kg/h), dose-dependently attenuated the increase in lung vascular permeability 30 min after CVF injection. Furthermore, sivelestat at 1 mg/kg/h almost totally prevented the increase in protein concentration in the bronchoalveolar lavage fluid without affecting lung neutrophil accumulation. These results suggest that neutrophil elastase is an important mediator in complement-mediated acute lung injury.

Exercise-induced neutrophil activation in claudicants: a physiological or pathological response to exhaustive exercise?

To assess the effect of exhaustive exercise on neutrophil activation and degranulation in claudicants and controls. We investigated the hypothesis that neutrophil activation and degranulation are normal responses to exhaustive exercise in healthy patients. This was a controlled experimental two-group study. Exercise was performed using a fixed workload treadmill test. Neutrophil activation was assessed by flow cytometry of whole blood labelled with anti-CD11b mouse IgG, and neutrophil degranulation in terms of plasma elastase measured by enzyme-linked immunosorbent assay. Twenty-eight claudicants with stage 1 chronic leg ischaemia, and 22 healthy controls were recruited. Blood and urine samples were collected before and after treadmill exercise. Claudicants exercised to their maximum walking distance, and controls at a higher "fatigue" workload for a maximum of 20 min. Exercise produced a brief but significant neutrophilia in both groups. Neutrophil CD11b expression increased significantly after exercise only in the claudicants, and was associated with a significant rise in plasma neutrophil elastase. These indices remained unchanged in the control group at all time points despite exercise at a fatigue level. The inflammatory response associated with exercise in claudicants is not simply a physiological response to exhaustive exercise.

Effect of collection and preprocessing methods on neutrophil elastase plasma concentrations.

Elevated plasma levels of the elastase alpha 1-proteinase inhibitor complex (E-alpha 1 PI) have been proposed as a marker of bacterial infection and neutrophil activation. Liberation of elastase from neutrophils after collection of blood may cause falsely elevated results. Collection methods have not been validated for critically ill neonates and children. We evaluated the influence of preanalytical methods on E-alpha 1 PI results including the recommended collection into EDTA tubes. First, we compared varying acceleration speeds and centrifugation times. Centrifugation at 1550 g for 3 min resulted in reliable preparation of leukocyte free plasma. Second, we evaluated all collection tubes under consideration for absorption of E-alpha 1 PI. Finally, 12 sets of samples from healthy adults and 42 sets obtained from critically ill neonates and children were distributed into the various sampling tubes. Samples were centrifuged within 15 min of collection and analyzed with a new turbidimetric assay adapted to routine laboratory analyzers. One of the two tubes containing a plasma-cell separation gel absorbed 22.1% of the E-alpha 1 PI content. In the remaining tubes without absorption of E-alpha 1 PI no differences were observed for samples from healthy adult patients. However, in samples from critically ill neonates or children, significantly higher results were obtained for plain Li-heparin tubes (mean = 183 micrograms/L), EDTA tubes (mean = 93 micrograms/L), and citrate tubes (mean = 88.5 micrograms/L) than for the Li-hep tube with cell-plasma separation gel and no absorption of E-alpha 1 PI (mean = 62.4 micrograms/L, p < 0.01). Contrary to healthy adults, E-alpha 1 PI results in plasma samples from critically ill neonates and children depend on the type of collection tube.

Suppression of plasma neutrophil elastase–α1-anti-proteinase complex by adequate replacement therapy in a patient with acquired hypogammaglobulinemia

J Allergy Clin Immunol 1997;100:553-5.

A human urinary protease inhibitor (Ulinastatin) inhibits neutrophil extracellular release of elastase during cardiopulmonary bypass

Objectives: To determine the benefits of a human urinary protease inhibitor (ulinastatin) on postoperative pulmonary dysfunction associated with neutrophil activation during cardiopulmonary bypass. Design: A prospective, randomized, clinical study Setting: The study was performed at Keio University Hospital, Tokyo. Participants: Eighteen adult patients scheduled for primary cardiac surgery. Interventions: The patients were randomly assigned either to the control group (n = 8) or to the group (n = 10) receiving ulinastatin (600,000 U in total). Measurements and Main Results: Human neutrophil ability to release elastase in response to N-formyl- l-methionyl-Lleucyl- l-phenylalanine (fMLP) in vitro was measured before and after cardiopulmonary bypass, together with plasma levels of neutrophil elastase complex, interleukin-8, and C3a. Intrapulmonary shunt fraction was then calculated. Neutrophil elastase release in response to fMLP significantly increased in the control group, but remained unchanged in the ulinastatin group. In addition, ulinastatin minimized the increase of plasma neutrophil elastase, independently of the production of interleukin-8 or C3a. Simultaneously, ulinastatin ameliorated the increase of intrapulmonary shunt, which was correlated with extracellular elastase release. Conclusions: Ulinastatin attenuated the elevation of fMLPinduced elastase release, which was associated with the deterioration of gas exchange during cardiopulmonary bypass. The administration of this agent has a potential to lessen the risk of postperfusion lung injury.

Increased neutrophil elastase, persistent intravascular coagulation, and decreased fibrinolytic activity in patients with posttraumatic acute respiratory distress syndrome.

To investigate the role of plasma neutrophil elastase (elastase-alpha1-proteinase inhibitor complex), plasminogen activator inhibitor-1 (PAI-1), and disseminated intravascular coagulation (DIC) in patients with posttraumatic acute respiratory distress syndrome (ARDS) and to explore the time course of the changes of these factors after trauma, we performed a prospective case-control study. The study subjects consisted of 41 trauma patients, 5 with ARDS, 7 at risk for but not developing the syndrome, and 29 control patients without or with no risk for ARDS. Plasma neutrophil elastase, PAI-1 activity, and PAI-1 antigen concentration were measured on the day of the injury and on days 1, 3, and 5 after admission. DIC was measured on the basis of the DIC score. The results of these measurements and demographic data were compared among the three groups. Neutrophil elastase, PAI-1 activity, and PAI-1 antigen concentration for the ARDS patients continued to be markedly high until the fifth day of admission, and the values on the fifth day were significantly higher than those of the other two groups. All patients with ARDS developed DIC. A decrease in the DIC score was found for the control patients and also for the patients at risk for ARDS; however, for the patients with ARDS, the DIC score did not improve during the study period (p = 0.5809). We provide precise information on the time course of neutrophil elastase, PAI-1, and DIC in trauma patients with ARDS and those at risk of developing this syndrome. Neutrophil activation and persistent intravascular coagulation as well as impaired fibrinolysis may play a role in the pathogenesis of posttraumatic ARDS.

The regulation of neutrophil activation and adhesion during femorodistal bypass surgery

To determine the effect that revascularising chronic critically ischaemic legs has no neutrophil activation and adhesion. Prospective clinical study. University Hospital. Twenty-five patients, 16 men and nine women undergoing femorodistal surgery. Venous blood assays for neutrophils expression of CD11b, neutrophil adhesion, and the plasma concentration of the shed endothelial adhesion receptor, soluble intracellular adhesion molecule 1 (sICAM-1). Urinary microalbuminaemia was measured and expressed as an albumin/creatinine ratio (ACR), as a marker of vascular permeability and plasma neutrophil elastase as evidence of neutrophil activation. Venous blood was taken preoperatively, during surgery and for the first 7 days postoperatively. Neutrophil CD11b expression fell following reperfusion of the limb (21.4 mcf to 9.7 mcf, p < 0.02 Mann Whitney U-test) as did neutrophil adhesion (preop. 75% adhesion, postop. 28% p < 0.01). However, the plasma elastase levels rose from 95 micrograms/l to 345 micrograms/l at 4 h and the ACR increased from 5.3 mg/ml to 304.2 mg/ml. The concentration of sICAM-1 fell following reperfusion (p < 0.04). The change in CD11b, sICAM-1 and adhesion may represent a normal immunological response to ischaemia/reperfusion.

N-Acetylcysteine pretreatment of cardiac surgery patients influences plasma neutrophil elastase and neutrophil influx in bronchoalveolar lavage fluid

N-Acetylcysteine pretreatment of cardiac surgery patients influences plasma neutrophil elastase and neutrophil influx in bronchoalveolar lavage fluid

Neutrophil activation in chronic liver disease.

To assess the relationship between neutrophil activation and indices of disease severity in patients with chronic liver disease. Plasma neutrophil elastase was measured by radioimmunoassay as a marker of neutrophil activation, and disease severity assessed by standard clinical, biochemical, haematological and histological techniques. Eighty-eight patients with chronic liver disease were studied, Thirty-nine had alcohol-induced liver disease (ALD), 18 autoimmune chronic hepatitis, 13 cryptogenic cirrhosis, seven primary biliary cirrhosis, six primary sclerosing cholangitis, three haemochromatosis and two secondary biliary cirrhosis. Seventy-three patients were cirrhotic and 15 were non-cirrhotic, confirmed by biopsy. Levels of neutrophil elastase were raised in Childs C cirrhotic patients with ALD compared with Childs A or B patients with ALD (P < 0.01), Childs A or B patients with non-ALD (P < 0.01), and Childs C patients with non-ALD (P = 0.02). In patients with ALD, neutrophil elastase correlated with prothrombin time (r = 0.679, P = 0.001), bilirubin (r = 0.587, P < 0.001), Child-Pugh score (r = 0.546, P < 0.001) and inversely with serum albumin (r = -0.511, P < 0.001). In patients with non-ALD, there were no correlations with the measurements of with transaminase levels. Neutrophil activation, as measured by plasma neutrophil elastase, is a marker of disease severity in patients with alcohol-induced chronic liver damage, but not in those with other causes of liver disease.

Leukopenia and rheological anomalies in leukocytes during hemodialysis in patients with chronic renal failure.

In order to clarify the relation between leukopenia during hemodialysis and leukocyte adhesiveness, the number of circulating leukocytes, their filterability through 5 micron diameter pores, and the concentration of neutrophil elastase in plasma were measured in peripheral blood collected at the beginning of hemodialysis (dialyzer, cuprophane membrane), 15 min into dialysis, and end of dialysis (duration of dialysis, 180 min) in 15 patients with chronic renal failure. Leukopenia was most marked at 15 min in all patients. In accordance with the change in number of circulating leukocytes, the filtration time of the leukocytes, as determined by a modification of the Nuclepore filtration method (filtered blood volume 0.5 ml, leukocyte count 2,500 microliters, suction pressure 10 cm H2O temperature 37 degrees C) was significantly longer at 15 min versus the beginning and end of the dialysis (p < 0.005 and p < 0.025, respectively). Addition of the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP; 20 nM), to the suspensions immediately increased the leukocyte filtration time. Such FMLP-induced increases were significantly greater at 15 min versus the beginning of dialysis (p < 0.05). This heightened sensitivity of cells to FMLP appeared to persist until the end of dialysis (p < 0.05 versus the beginning). Plasma levels of neutrophil elastase were highest at the end of dialysis versus those at the beginning and after 15 min (both p < 0.005). Results suggest that the changes in filterability of leukocytes may be related to decreases in their number in the circulation. Neutrophil elastase appeared to accumulate in plasma so that its maximal value at the end of dialysis would reflect the preceding changes in leukocyte rheology.

Relationship between plasma neutrophil elastase and respiratory index of patients who had undergone cardiac surgery with cardiopulmonary bypass

To evaluate the effects of cardiopulmonary bypass (CPB) on the release of polymorphonuclear leukocyte elastase (PMN-E) and postoperative pulmonary function, the perioperative plasma levels of PMN-E in α1-antitrypsin complex (EAC) and hydrogen peroxide concentration in the expired breath were measured in eight patients who underwent cardiac surgery with CPB, and the relationship between EAC levels and the respiratory index (RI) was studied. Although PMN, EAC, and the ratio of EAC to neutrophil (E/N) were elevated significantly after surgery, alveolar-arterial oxygen difference (A-aDO2) and respiratory index (A-aDO2/PaO2) did not change when compared with those of the preoperative period. Hydrogen peroxide concentration in the expired breath also did not change (below 2.5 μmol·l(-1)) during the perioperative period. These results suggest that the elevation of EAC immediately after cardiac surgery using CPB, which lasted less than 2h, was not a cause of postoperative pulmonary disorder. However, there was a significant positive correlation between E/N ratio and respiratory index (r=0.67,P<0.01). Thus excessive release of PMN-E during CPB may be implicated in the etiology of postoperative respiratory dysfunction.

Relationship between plasma neutrophil elastase and respiratory index of patients who had undergone cardiac surgery with cardiopulmonary bypass

Relationship between plasma neutrophil elastase and respiratory index of patients who had undergone cardiac surgery with cardiopulmonary bypass

Microcirculatory aspects of venous ulceration.

Articles were identified from a literature search based on Index Medicus from 1983 onwards with additional, as yet, unpublished data obtained directly from ongoing research at The Middlesex Hospital Vascular Laboratory. Original scientific articles were selected if they addressed the mechanisms causing venous ulceration in relation to the events in the microcirculation. To review the mechanisms proposed recently to explain the pathogenesis of venous ulceration. Recent data suggest that there is a systemic inflammatory response associated with the presence of venous disease in the lower limb, as indicated by measuring plasma neutrophil elastase and lactoferrin. In volunteers without venous disease white cell activation may be produced by experimental venous hypertension lasting 30 minutes, produced by applying a venous tourniquet to the lower limb or by standing without moving for 30 minutes. Inflammatory mechanisms play a significant role in the pathogenesis of venous disease but the exact mechanisms producing venous ulceration remain to be elucidated.

Enhanced attachment and elastase-releasing capacity of neutrophils after surgery

Perioperative changes in neutrophil attachment level and neutrophil elastase-releasing capacity were examined in patients who underwent surgery for either esophageal or gastric cancer. The neutrophil attachment level was significantly increased in both groups to approximately three times that of the preoperative value. The elastase-releasing capacity of nonstimulated neutrophils was not significantly changed, but it was significantly increased in neutrophils stimulated by N-formyl-L-methipnyl-L-leucyl-L-phenylalanine (FMLP). Moreover, both neutrophil attachment and elastase-releasing capacity of FMLP-stimulated neutrophils were more enhanced in patients with postoperative complications than in patients without complications. Peak levels of serum interleukin 6, serum α1 proteinase inhibitor, and plasma neutrophil elastase were also significantly higher in patients with postoperative complications than in patients without. These results suggest that during the postoperative period, neutrophils may be primed and activated in response to inflammatory mediators such as cytokines, and that such an alteration of neutrophil functions may reflect the extent of inflammation and may, at times, be implicated in postoperative complications.