PURPOSE: Parenteral nutrition is given to infants who tempararily cannot take oral feeding adequately. A lipid emulsion is added to the parenteral to supply essential fatty acids. In neonatal sepsis, elastase from azuropilic granules of the neutrophils is released and rapidly bound to alpha1-Proteinase Inhibitor(alpha1-PI). The lipid emulsion has been noted to markedly inhibit chemotaxis of neutrophils, so we to measured the levels of Elastase-alpha1-Proteinase Inhibitor(E-alpha1-PI) complex to evaluate the effect of intralipid infusions on the neutrophil in newborns with sepsis. METHODS: This study evaluated 8 patients with neonatal sepsis and 12 normal newborns. We measured E-alpha1-PI complex levels in the serum of these patients by ELISA methods. RESULTS: Before infusion with lipid solution, patients with neonatal sepsis had significantly increased levels of E-alpha1-PI complex in comparison with those of vaginally delivered normal newborns. E-alpha1-PI complex levels were significantly decreased after lipid infusions of 0.5g/kg per day, but there was no further significant decrease with higher doses of the infusate. CONCLUSION: We observed the suppression neutrophil elastase levels by lipid infusions in newborn with sepsis. These results suggest that there were no appropriate chemotatic effects of neutrophil in newborn with sepsis. Therefore, we considered whether the lipid infusion was stopped if the newborn with sepsis was infused parenteral nutrition with intralipid.
Chemotaxis ; Enzyme-Linked Immunosorbent Assay ; Fatty Acids, Essential ; Humans ; Infant ; Infant, Newborn* ; Leukocyte Elastase ; Neutrophils ; Pancreatic Elastase* ; Parenteral Nutrition ; Sepsis

PURPOSE: Kawasaki disease is notorious for coronary arterial complication which is usually developed as a febrile disease in early childhood. Increased polymorphonucleus(PMN) cell levels in acute phases may be associated with the pathophysiology of Kawasaki disease. We studied the relationship between coronary arterial dilatation and elastase activity which was excreted from PMN cell and roles as an important factor for vasculitis. METHODS: Ten patients diagnosed with Kawasaki disease in Yonsei University Medical Center were examined between November, 2001 and January, 2002. In addition, 15 patients with other febrile diseases were also examined. Echocardiography was done in patients with Kawasaki disease on the first day of admission and four weeks after the onset of the disease. At each time, venous samples were drawn and separated into plasma and leukocytes. In patients with other febrile disease, samples were drawn on admission. Elastase activities in plasma and neutrophil extracts were measured. RESULTS: The significant increased plasma elastase activity, 6.19+/-0.74 U/mL, found in Kawasaki disease patients compared with the other febrile disease patients, 4.86+/-1.17 U/mL(P<0.05). And there was no significance between the above two diseases in terms of the elastase activity in neutrophil extracts. The relationship between initial elastase activity and the coronary arterial complication which was shown in subacute phase wasn't significant. CONCLUSION: Plasma elastase activity was increased in Kawasaki disease significantly, but the initial plasma elastase activity in the acute phase could not reflect the range of coronary arterial complication.
Academic Medical Centers ; Dilatation* ; Echocardiography ; Humans* ; Leukocyte Elastase* ; Leukocytes ; Mucocutaneous Lymph Node Syndrome* ; Neutrophils* ; Pancreatic Elastase ; Plasma ; Vasculitis

BACKGROUND: Interleukin-1 (IL-1) and neutrophil appear to contribute to the pathogenesis of acute respiratory distress syndrome (ARDS). Elastase, as well as reactive oxygen species released from activated neutrophil, are thought to play pivotal roles in the experimental models of acute lung leak. This study investigated whether ICI 200,355, a synthetic elastase inhibitor, can attenuate acute lung injury induced by IL-1 in rats. MATERIALS AND METHODS: We intratracheally instilled either saline or IL-1 with and without treatment of ICI 200,355 in rats. Lung lavage neutrophils, lung lavage cytokine-induced neutrophil chemoattractant(CINC) concentration, lung lavage protein concentration, lung myeloperoxidase(MPO) activity and lung leak index were measured at 5 hours of intratracheal treatment. RESULTS: In rats given IL-1 intratracheally, lung lavage neutrophils, lung lavage CINC concentration, lung lavage protein concentration, lung MPO activity and lung leak index were higher. Intratracheal ICI 200,355 administration decreased lung lavage neutrophils, lung MPO activity and lung leak index, respectively, but did not decreased lung lavage CINC concentration. CONCLUSION: These results suggest that ICI 200,355 decreases lung inflammation and leak without decreasing lung lavage CINC concentration in rats given IL-1 intratracheally.
Acute Lung Injury* ; Animals ; Bronchoalveolar Lavage ; Interleukin-1* ; Leukocyte Elastase* ; Lung ; Models, Theoretical ; Neutrophils* ; Pancreatic Elastase ; Pneumonia ; Rats* ; Reactive Oxygen Species ; Respiratory Distress Syndrome, Adult

BACKGROUND: Interleukin-1 (IL-1) and neutrophil appear to contribute to the pathogenesis of acute respiratory distress syndrome (ARDS). Elastase, as well as reactive oxygen species released from activated neutrophil, are thought to play pivotal roles in the experimental models of acute lung leak. This study investigated whether ICI 200,355, a synthetic elastase inhibitor, can attenuate acute lung injury induced by IL-1 in rats. MATERIALS AND METHODS: We intratracheally instilled either saline or IL-1 with and without treatment of ICI 200,355 in rats. Lung lavage neutrophils, lung lavage cytokine-induced neutrophil chemoattractant(CINC) concentration, lung lavage protein concentration, lung myeloperoxidase(MPO) activity and lung leak index were measured at 5 hours of intratracheal treatment. RESULTS: In rats given IL-1 intratracheally, lung lavage neutrophils, lung lavage CINC concentration, lung lavage protein concentration, lung MPO activity and lung leak index were higher. Intratracheal ICI 200,355 administration decreased lung lavage neutrophils, lung MPO activity and lung leak index, respectively, but did not decreased lung lavage CINC concentration. CONCLUSION: These results suggest that ICI 200,355 decreases lung inflammation and leak without decreasing lung lavage CINC concentration in rats given IL-1 intratracheally.
Acute Lung Injury* ; Animals ; Bronchoalveolar Lavage ; Interleukin-1* ; Leukocyte Elastase* ; Lung ; Models, Theoretical ; Neutrophils* ; Pancreatic Elastase ; Pneumonia ; Rats* ; Reactive Oxygen Species ; Respiratory Distress Syndrome, Adult

OBJECTIVES: Alpha1-antitrypsin (AAT) is the main inhibitor of human neutrophil elastase, and plays a role in counteracting the tissue damage caused by elastase in local inflammatory conditions. The study evaluated the involvement of AAT in nasal allergic inflammation. METHODS: Forty subjects with mono-sensitization to Dermatophagoides pteronyssinus (Dpt) were enrolled. Twenty allergic rhinitis patients frequently complained of nasal symptoms such as rhinorrhea, stuffiness, sneezing, and showed positive responses to the nasal provocation test (NPT) with Dpt (Group I). The other 20 asymptomatic patients showed sensitization to Dpt but negative NPT (Group II). The levels of AAT, eosinophil cationic protein (ECP), and Dpt-specific IgA antibodies were measured in the nasal lavage fluids (NLFs), collected at baseline, 10 minutes, 30 minutes, 3 hours, and 6 hours after the NPT. Nasal mucosa AAT expression was evaluated with immunohistochemical staining from Group I and Group II. RESULTS: At baseline, only the Dpt-specific IgA level was significantly increased in the NLFs of Group I compared with Group II, while ECP and AAT levels were not significantly different between two groups. After Dpt provocation, AAT, ECP, and Dpt-specific IgA levels were significantly increased in the NLFs of Group I during the early and late responses. The protein expression level of AAT was mostly found in the infiltrating inflammatory cells of the nasal mucosa, which was significantly increased in Group I compared to Group II. CONCLUSION: The increment of AAT showed a close relationship with the activation of eosinophils induced by allergen-specific IgA in the NLFs of patients with allergic rhinitis after allergen stimulation. These findings implicate AAT in allergen-induced nasal inflammation.
Antibodies ; Dermatophagoides pteronyssinus ; Eosinophil Cationic Protein ; Eosinophils ; Humans ; Immunoglobulin A ; Inflammation ; Leukocyte Elastase ; Nasal Lavage Fluid ; Nasal Mucosa ; Nasal Provocation Tests ; Pancreatic Elastase ; Rhinitis ; Rhinitis, Allergic, Perennial ; Sneezing

OBJECTIVES: Alpha1-antitrypsin (AAT) is the main inhibitor of human neutrophil elastase, and plays a role in counteracting the tissue damage caused by elastase in local inflammatory conditions. The study evaluated the involvement of AAT in nasal allergic inflammation. METHODS: Forty subjects with mono-sensitization to Dermatophagoides pteronyssinus (Dpt) were enrolled. Twenty allergic rhinitis patients frequently complained of nasal symptoms such as rhinorrhea, stuffiness, sneezing, and showed positive responses to the nasal provocation test (NPT) with Dpt (Group I). The other 20 asymptomatic patients showed sensitization to Dpt but negative NPT (Group II). The levels of AAT, eosinophil cationic protein (ECP), and Dpt-specific IgA antibodies were measured in the nasal lavage fluids (NLFs), collected at baseline, 10 minutes, 30 minutes, 3 hours, and 6 hours after the NPT. Nasal mucosa AAT expression was evaluated with immunohistochemical staining from Group I and Group II. RESULTS: At baseline, only the Dpt-specific IgA level was significantly increased in the NLFs of Group I compared with Group II, while ECP and AAT levels were not significantly different between two groups. After Dpt provocation, AAT, ECP, and Dpt-specific IgA levels were significantly increased in the NLFs of Group I during the early and late responses. The protein expression level of AAT was mostly found in the infiltrating inflammatory cells of the nasal mucosa, which was significantly increased in Group I compared to Group II. CONCLUSION: The increment of AAT showed a close relationship with the activation of eosinophils induced by allergen-specific IgA in the NLFs of patients with allergic rhinitis after allergen stimulation. These findings implicate AAT in allergen-induced nasal inflammation.
Antibodies ; Dermatophagoides pteronyssinus ; Eosinophil Cationic Protein ; Eosinophils ; Humans ; Immunoglobulin A ; Inflammation ; Leukocyte Elastase ; Nasal Lavage Fluid ; Nasal Mucosa ; Nasal Provocation Tests ; Pancreatic Elastase ; Rhinitis ; Rhinitis, Allergic, Perennial ; Sneezing

Human neutrophil elastase (HNElastase, EC 3.4.21.37), a causative factor of inflammatory diseases, was purified by Ultrogel AcA54 gel filtration and CM-Sephadex ion exchange chromatography. HNElastase was inhibited by phenylbutazone in a concentration dependent manner up to 0.4 mm, but as the concentration increased, the inhibitory effect gradually diminished. Binding of phenylbutazone to the human neutrophil elastase caused strong Raman shifts at 200, 440, and 1194 cm-1. The peak at 1194 cm-1 might be evidence of the presence of -N=N-PHI radical. The core area of the elastase, according to the visual molecular model of human neutrophil elastase, was structurally stable. A deeply situated active center was at the core area surrounded by hydrophobic amino acids. Directly neighboring the active site was one positively charged atom and two atoms carrying a negative charge, which enabled the enzyme and the drug to form a strong interaction. Phenylbutazone may form a binding, similar to a key & lock system to the atoms carrying opposite charges near the active site of the enzyme molecule. Furthermore, the hydrophobicity of the surrounding amino acid near the active site seemed to enhance the binding strength of phenylbutazone. Binding of phenylbutazone near the active site may cause masking of the active site, preventing the substrate from approaching the active site and inhibiting elastase activity.
Amino Acids ; Catalytic Domain ; Chromatography, Gel ; Chromatography, Ion Exchange ; Humans* ; Hydrophobic and Hydrophilic Interactions ; Leukocyte Elastase* ; Masks ; Models, Molecular ; Neutrophils* ; Pancreatic Elastase ; Phenylbutazone*

No abstract available
Acute Lung Injury* ; Pancreatic Elastase*

OBJECTIVETo investigate the change of secretory leukocyte protease inhibitor (SLPI) and elastase (EA) in the different stages of periodontal inflammation and to evaluate the possibility of the two proteins as saliva markers reflecting overall periodontal health status.

METHODSUnstimulated whole saliva were collected from 86 subjects (divided into 4 groups as healthy, gingivitis, moderate periodontitis and severe periodontitis). Fifteen patients with moderate or severe periodontitis were only given scaling and root planning (SRP). Whole saliva was collected and clinical patameters were recorded at baseline and four weeks after the treatment. SLPI concentrations were determined with enzyme linked immunosorbent assay (ELISA) systems, while EA with low-molecular-weight substrate reaction.

RESULTSThere were no statistical differences of SLPI concentrations among four groups (P > 0.05). However, EA activities in moderate periodontitis and severe periodontitis groups [0.077 (0.060) and 0.077 (0.489)] were higher than in healthy and gingivitis group [0.058 (0.028) and 0.058 (0.024)] (P < 0.05). SLPI only showed a weak negative correlation with age (r = -0.301, P < 0.05), rather than with EA or clinical parameters. In 15 patients with chronic periodontitis the mean concentration of SLPI and EA activity was 2.031 (2.449) µg/L and 0.075 (0.118), and both decreased significantly to 1.405 (0.659) µg/L and 0.055 (0.028) respectively 4 weeks after SRP.

CONCLUSIONSAfter SRP, the decrease of SLPI concentration and EA activity in saliva may reflect the periodontal inflammation subsiding. SLPI in saliva was not correlated with the development of periodontal inflammation.

Adult ; Chronic Periodontitis ; metabolism ; therapy ; Dental Plaque Index ; Dental Scaling ; Female ; Gingivitis ; metabolism ; Humans ; Male ; Middle Aged ; Pancreatic Elastase ; metabolism ; Periodontal Index ; Periodontitis ; metabolism ; therapy ; Root Planing ; Saliva ; metabolism ; Secretory Leukocyte Peptidase Inhibitor ; metabolism ; Young Adult

PURPOSE: The aim of this study was to evaluate the clinical significance of inflammatory biomarkers in acute infectious diarrhea among children. METHODS: Clinical parameters including fever, bacterial and viral etiology based on stool culture and multiplex polymerase chain reaction, and nine biomarkers including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and leukocytes in blood and calprotectin, lactoferrin, myeloperoxidase, polymorphonuclear elastase, leukocytes, and occult blood in feces were evaluated in children who were hospitalized due to acute diarrhea without underlying disease. RESULTS: A total of 62 patients were included. Among these patients, 33 had fever, 18 showed bacterial infections, and 40 patients were infected with 43 viruses. Of all the biomarkers, CRP was significantly correlated with fever (p<0.001). CRP, ESR, calprotectin, lactoferrin, myeloperoxidase, fecal leukocytes, and occult blood were significantly associated with infection with bacterial pathogens (p<0.001, p=0.04, p=0.03, p=0.003, p=0.02, p=0.03, p=0.002, respectively). The combination of CRP and fecal lactoferrin at their best cut-off values (13.7 mg/L and 22.8 µg/mL, respectively) yielded a sensitivity of 72.2%, and a specificity of 95.5% for bacterial etiology compared with their individual use. CONCLUSION: Blood CRP is a useful diagnostic marker for both fever and bacterial etiology in acute pediatric diarrhea. The combination of CRP and fecal lactoferrin yields better diagnostic capability for bacterial etiology than their use alone for acute diarrhea in children without underlying gastrointestinal disease.
Bacterial Infections ; Biomarkers ; Blood Sedimentation ; C-Reactive Protein ; Child ; Diarrhea ; Feces ; Fever ; Gastrointestinal Diseases ; Humans ; Lactoferrin ; Leukocyte L1 Antigen Complex ; Leukocytes ; Multiplex Polymerase Chain Reaction ; Occult Blood ; Pancreatic Elastase ; Peroxidase ; Sensitivity and Specificity