Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to investigate whether platelets are activated and release their products in the human lung after antigen challenge. Using subsegmental antigen challenge as a model of asthma, bronchoalveolar lavage fluids from ragweed-allergic asthmatic subjects were assayed for the alpha granule products, platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG), prior to challenge (baseline) and at 5 min and 19 h after challenge with ragweed antigen. Airway segments challenged with normal saline were used as controls. Five minutes after antigen challenge, levels of platelet products in BAL fluid were not elevated from baseline or normal saline control levels. However, 19 h after antigen challenge, a 10-fold increase in platelet products in BAL fluids was found. The mean PF4 levels increased from baseline and saline control values of less than 1.0 to 7.2 ng/ml (p less than 0.05) 19 h after antigen challenge. beta-TG increased from baseline and control levels of less than 1.0 to 6.6 ng/ml (p less than 0.05). Elevations in PF4 and beta-TG were highly correlated with each other (r = 0.98, p less than 0.0001). Levels of platelet products during the 19-h response correlated with albumin, with kinins, with the prostaglandins 6-keto-PGF1 alpha, PGE2, and PGF2 alpha, and with the eosinophil-derived proteins, eosinophil-derived neurotoxin and eosinophil peroxidase. We conclude that platelet activation in the lung is a feature of the late inflammatory response to antigen challenge and that platelets may play an important role in allergic inflammation and asthma.
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PMID:Platelet activation in the lung after antigen challenge in a model of allergic asthma. 153 19

Eosinophils are found in the blood and tissues of patients with allergic diseases such as asthma, allergic rhinitis and also atopic dermatitis. The number of eosinophils in the diseased tissue generally correlates with the expression of clinical symptoms. Originally, the eosinophil was regarded as having an exclusively protective role, for example in host defense against parasites. More recently, the eosinophil is recognized as being a pro-inflammatory cell that can mediate allergic disease. The eosinophil is active in inflammation through the release of granule proteins and the synthesis and release of inflammatory mediators. The important eosinophil granule proteins are major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil derived neurotoxin (EDN) and eosinophil peroxidase (EPO). These proteins have toxic effects on the surrounding tissue. Of additional importance for the allergic inflammatory reactions are membrane-derived mediators such as leukotriene C4 (LTC4), platelet activating factor (PAF) and Charcot-Leyden crystals. These mediators are synthesized and released after eosinophil activation, and act toxic on surrounding cells. Eosinophils are active in asthma, and increased numbers and eosinophil-derived mediator concentrations have been documented in bronchial biopsies, BAL and sputum. In addition, eosinophil granule proteins and inflammatory mediators are found in nasal secretions in allergic rhinitis. In atopic dermatitis one finds activated eosinophils and depositions of eosinophil granule proteins in skin biopsies. Eosinophils are not only active in mediating allergic inflammation, but interact in cellular networks with antigen presenting cells (APC), mast cells, and T lymphocytes. These other cells influence eosinophil maturation, mobilization, tissue localization and activation.
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PMID:[Eosinophilic granulocytes and their significance in allergic diseases]. 153 93

Previous studies from our laboratory have demonstrated a temporal relationship between eosinophil influx into the airways and the onset of airway hyperresponsiveness to inhaled methacholine. The purpose of the present study was to extend this observation by evaluating changes in airway cellular composition and measuring the levels of granulocyte-derived mediators recovered in BAL fluid during the onset and recovery from antigen-induced airway hyperresponsiveness. Airway cellular composition, airway responsiveness to inhaled methacholine and the levels of BAL fluid EPO and MPO were monitored over a 32 day study in eight adult male Ascaris suum sensitive cynomolgus monkeys. Repeated Ascaris suum inhalation (nine challenges during days 0-21) resulted in a selective, sustained airway eosinophilia that was temporally related with the onset and maintenance of airway hyperresponsiveness (r = 0.67, P less than 0.001). The level of BAL eosinophil-derived EPO was increased and remained elevated concurrent with the increase in airway eosinophils and airway responsiveness. During the recovery phase (days 22-32) the actual number of eosinophils remained elevated, while BAL EPO levels were significantly decreased. The recovery phase was also associated with a transient increase in the number of BAL neutrophils and MPO concentration. We conclude that the number and state of activation of airway eosinophils directly correlate with the onset and maintenance of airway hyperresponsiveness. Recovery from airway hyperresponsiveness is associated with a decrease in eosinophil activation and a transient increase in the number of activated neutrophils.
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PMID:The onset and recovery from airway hyperresponsiveness: relationship with inflammatory cell infiltrates and release of cytotoxic granule proteins. 157 22

The proliferation of alveolar macrophages in 47 patients with pulmonary sarcoidosis was investigated using immune peroxidase stains with the monoclonal antibody Ki-67. In patients suffering from sarcoidosis, a significantly elevated number of Ki-67-positive alveolar macrophages was observed. The number of proliferating alveolar macrophages showed a significant positive correlation both with the number of lymphocytes in the BAL fluid and with the T4/T8 quotient in the BAL fluid of sarcoidosis patients.
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PMID:[Proliferation of alveolar macrophages in pulmonary sarcoidosis correlates with markers of lymphocyte activity in bronchoalveolar lavage fluid]. 197 97

A monoclonal antibody has been made to a peptide that is released by human alveolar macrophages. This enzyme-releasing peptide (ERP) causes neutrophils to secrete azurophilic granule enzymes. Normal subjects, patients with pulmonary fibrosis, and patients with sarcoidosis had similar concentrations of this peptide in their bronchoalveolar lavage fluids. However, patients with the adult respiratory distress syndrome (ARDS) had about 2.7 times higher concentrations in their lavage fluids. The enzyme-releasing activity in the lavage fluids was significantly correlated with 2 indices of the severity of the clinical illness in patients with ARDS, the APACHE score, and the chest radiograph score. The correlation was diminished or ablated by removing the peptide with the monoclonal antibody bound to staphylococcal Sepharose 4B. This peptide accounted for 62.08% (SD = 15.88%) of the enzyme-releasing activity in fluids from lungs of patients with ARDS and 86.39% (SD = 24.46%) of the activity in fluids from lungs of normal control subjects. Therefore, ERP is the major neutrophil enzyme-releasing agent in the bronchoalveolar lavage fluid from patients with ARDS and from normal persons. There was a significant correlation between the neutrophil enzyme-releasing activity and the ERP concentrations in BAL of patients with ARDS. These observations suggest that modulation of neutrophil function by ERP significantly controls the protease and peroxidase loads in the lungs of patients with ARDS.
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PMID:A peptide from alveolar macrophages that releases neutrophil enzymes into the lungs in patients with the adult respiratory distress syndrome. 284 27

1. Serial bronchoalveolar lavages were performed on a subhuman primate (Macacus cynomolgus) in order to give an experimental model for silicosis. 2. We have measured glycosidases, proteases, peroxidase and antiproteases of the BAL fluids from seven normal monkeys. 3. The results obtained were similar to those found in human control BAL fluids. 4. For monkeys, the repetition of the bronchoalveolar procedure does not seem to have an important influence on the values obtained. 5. The present results will now permit sequential follow up studies during the course of experimental silicosis.
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PMID:Comparison of hydrolases, peroxidase and protease inhibitors in bronchoalveolar fluid from Macacus cynomolgus and human controls. 332 59

Characterizing lymphocyte subsets in bronchoalveolar lavage fluid (BALF) by flow cytometry (FC) proper gating of the lymphocyte subpopulation being analyzed is crucial. In order to test lymphocyte gate quality for the first time we used a DNA-dye to evaluate plasmamembrane integrity and thus to mark off fluorescent but not DNA-containing particles (eg, debris). A comparative prospective study between this newly developed FC technique and a standard peroxidase anti-peroxidase (PAP) method was performed. Samples of BALF from 50 patients with various pulmonary diseases were examined. After determination of the total cell yield, a differential cell count was performed. Subsequently, the immunophenotype of pan T lymphocyte CD3-, T-helper lymphocyte CD4-, and T-suppressor lymphocyte CD8-positive lymphocyte subsets was assessed with FC as well as with the PAP method. Both methods showed excellent correlation (CD3: r = 0.81; CD4: r = 0.97; CD8: r = 0.96; p < 0.05, respectively). Comparing the mean +/- SEM, FC tends to overestimate CD3+ cells (90.6 +/- 1.0% vs 85.8 +/- 1.3%). For CD4 (45.0 +/- 3.4% vs 44.4 +/- 3.4%) and CD8 (48.1 +/- 3.5% vs 46.7 +/- 3.5%), there was good agreement. In a clinical setting, the reliability of both methods was equivalent, and FC using a DNA-dye to test lymphocyte gate quality offered a rapid and reliable determination of lymphocyte subsets in BAL.
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PMID:Immunophenotyping of lymphocytes in bronchoalveolar lavage fluid. A new flow cytometric method vs standard immunoperoxidase technique. 763 85

The aim of this study was to evaluate the ability of alveolar inflammatory cells recovered by bronchoalveolar lavage from the lower respiratory tract of 17 smoking patients with or without emphysema to inactivate alpha 1-proteinase inhibitor (alpha 1-Pl). The presence of emphysema was determined and quantified using CT scan and was evidenced in 8 patients (Group 1), whereas 9 patients exhibited a normal CT scan (Group 2). Patients with emphysema had lower values of FEV1, DLCO, and resting PO2 and higher values of RV/TLC ratio than patients without emphysema. BAL analysis showed a higher percentage of neutrophils and of myeloperoxidase (MPO) in BAL fluid in Group 1 than in Group 2. Alveolar inflammatory cells stimulated or not with phorbol myristate acetate (PMA) were incubated for 45 min with purified alpha 1-Pl, and the results were expressed as a percentage of inactivation of alpha 1-Pl as evaluated by its inhibitory activity against porcine pancreatic elastase or human neutrophil elastase. In Group 2, unstimulated alveolar inflammatory cells inactivated only 3.3 +/- 0.7% alpha 1-Pl and stimulated cells inactivated only 5.4 +/- 1.1% alpha 1-Pl. In marked contrast, in Group 1, a significant loss of the antielastase function of alpha 1-Pl was observed (p < 0.001) when alpha 1-Pl was incubated with unstimulated cells (24.2 +/- 8.9%) or stimulated cells (35 +/- 8.9%) from Group 1. The addition of catalase to the cell suspension was associated with a significant decrease in the inactivation of alpha 1-Pl (from 35 +/- 8.9 to 10.2 +/- 1.2%, Group 1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inactivation of alpha 1-proteinase inhibitor by alveolar inflammatory cells from smoking patients with or without emphysema. 838 10

In order to test the hypothesis that ozone (O3)-induced changes in lung function and respiratory tract injury/inflammation are greater in subjects with asthma than in normal subjects, we exposed 18 asthmatic subjects, on separate days, to O3 (0.2 ppm) and filtered air for 4 h during exercise. Symptom questionnaires were administered before and after exposure, and pulmonary function tests (FEV1, FVC, and specific airway resistance [SRaw]) were performed before, during, and immediately after each exposure. Fiberoptic bronchoscopy, with proximal airway lavage (PAL) of the isolated left main bronchus and bronchoalveolar lavage (BAL; bronchial fraction, the first 10 ml of fluid recovered) of the right middle lobe, was performed 18 h after each exposure. The PAL, bronchial fraction, and BAL fluids were analyzed for the following endpoints: total and differential cell counts; total protein, lactate dehydrogenase (LDH), fibronectin, interleukin-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF), myeloperoxidase (MPO), and transforming growth factor-beta (TGF beta 2) concentrations. We found a significant O3 effect on FEV1, FVC, SRaw (p < 0.04) and lower respiratory symptoms (p < 0.001) for the asthmatic subjects. Ozone exposure also significantly increased the percent neutrophils in PAL (p < 0.01); percent neutrophils, total protein, and IL-8 in the bronchial fraction (p < 0.001, p < 0.05, and p < 0.01, respectively); and the percent neutrophils, total protein, LDH, fibronectin, IL-8, GM-CSF, and MPO in BAL (p < 0.001, p < 0.01, p < 0.01, p < 0.001, p < 0.05, p < 0.01, and p < 0.001, respectively) for the asthmatic subjects. There were no significant differences in the lung function responses of the asthmatic subjects in comparison with a group of normal subjects (n = 81) previously studied using an identical protocol, although there was a trend toward a greater O3-induced increase in SRaw in the asthmatic subjects (p < 0.13). In contrast, the asthmatic subjects showed significantly greater (p < 0.05) O3-induced increases in several inflammatory endpoints (percent neutrophils and total protein concentration) in BAL as compared with normal subjects who underwent bronchoscopy (n = 20). Our results indicate that asthmatic persons may be at risk of developing more severe O3-induced respiratory tract injury/inflammation than normal persons, and may help explain the increased asthma morbidity associated with O3 pollution episodes observed in epidemiologic studies.
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PMID:Greater ozone-induced inflammatory responses in subjects with asthma. 868 Jun 87

Lung transplantation has become an accepted therapy for end-stage lung disease. Acute rejection of the transplanted hung still remains a major clinical problem since it decreases graft survival. Eosinophil cationic protein (ECP) from activated eosinophils, hyaluronan (HYA) from fibroblasts, and circulating intercellular adhesion molecule 1 (1CAM-1) have been associated with acute rejection in kidney and liver grafts. We investigated whether these, as well as other molecules, were increased in acute rejection of lung allografts. Serum and BAL fluid from 38 bronchoscopies performed in 9 single lung, 2 bilateral lung, and 4 heart-lung transplant patients were studied. Differential cell counts were made from the BAL fluid. Levels of ECP, myeloperoxidase (MPO), and HYA were used as indirect markers for activation of eosinophils, neutrophils, and fibroblasts, respectively. In addition, levels of circulating ICAM-1, cVCAM-1, and cE-selectin were analyzed. Twenty-two episodes with acute rejection were diagnosed. Of these, 7 were minimal, 13 were mild, and 2 were of moderate character. We found increased levels of ECP and HYA in BAL fluid during mild acute rejection of the allograft. Numbers of eosinophils were also increased. Activation of neutrophils or neutrophil numbers were not significantly increased. Levels of circulating ICAM-1, cVCAM-1, and cE-selectin did not differ between the groups. This retrospective study shows that measurements of ECP and HYA can give information about the inflammatory process present during acute rejection in patients who have undergone lung transplants. Analysis of cCAMS, however, appears to be of limited value as markers for acute rejection.
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PMID:Activation of eosinophils and fibroblasts assessed by eosinophil cationic protein and hyaluronan in BAL. Association with acute rejection in lung transplant recipients. 868 73


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