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)

Bronchoalveolar lavage fluid (BALF) cell profiles, interleukins 1 and 2, (IL-1 and IL-2) and soluble interleukin 2 receptor (IL-2R) levels from patients with pigeon breeders' disease (PBD) (n = 24) and asymptomatic pigeon breeders (n = 10) were compared with those from patients with active sarcoidosis (n = 11), inactive sarcoidosis (n = 10), idiopathic pulmonary fibrosis (n = 25) and normal subjects (n = 10). BALF total cells, lymphocytes and OKT4 receptor-bearing lymphocytes/ml were higher in PBD and active sarcoidosis compared with normals (P less than 0.02 all comparisons). In the asymptomatic pigeon breeders bronchoalveolar (BA) lymphocyte numbers/ml were higher than controls (P less than 0.01) producing a subclinical lymphocytic "alveolitis" in 80% of subjects, although compared with symptomatics, % OKT4 (helper) cell numbers were lower (P less than 0.05). OKT4/OKT8 ratios in both groups were normal, whereas in active sarcoidosis ratios were higher (P less than 0.05) but with considerable overlap. Mean levels of IL-1 and IL-2 were raised in the BALF from all groups compared with normals (P less than 0.01 all comparisons), IL-2 being higher in active sarcoidosis and IPF compared with PBD (P less than 0.01). There was no significant difference in detectable BALF soluble IL-2R between patient groups, although its levels correlated positively with IL-1 (22 paired samples from all groups (rs = 0.8, P less than 0.02) and negatively with % and T-lymphocytes/ml in PBD (rs = 0.75, P less than 0.02, rs less than 0.8, P less than 0.01). However, when BALF soluble IL-2R is expressed in terms of T lymphocytes/ml of epithelial lining fluid (ELF), asymptomatic pigeon breeders had significantly higher levels than their symptomatic counterparts (P less than 0.01). It is concluded that percentage lymphocytes [corrected] are similar in both groups of pigeon breeders, although those with PBD had increased numbers of OKT4 (helper) cells. Patients with active sarcoidosis could not be reliably differentiated from those with acute PBD on the basis of BAL cell profiles. Our results suggest that IL-1 leads to soluble IL-2R formation and that continued antigenic stimulation, as with inhaled pigeon allergens, results in a down regulation of BALF IL-2. Excess BALF soluble IL-2R on a cellular basis suggests a mechanism by which some pigeon breeders remain asymptomatic.
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PMID:Immunoregulatory proteins in bronchoalveolar lavage fluid. A comparative analysis of pigeon breeders' disease, sarcoidosis and idiopathic pulmonary fibrosis. 260 84

Previous studies have suggested that immunologic mechanisms may contribute to pathogeneic reactions in certain interstitial lung diseases. Cytolytic lymphocytes are major effector cells of the immune response that have not been extensively studied in these disorders. To investigate the role of activated cytolytic lymphocytes in IPF, we studied B-cell and monocyte/macrophage-depleted lymphocyte preparations isolated from BAL fluid and peripheral blood of patients with this disease (n = 10) and used a lectin-dependent cytotoxicity assay to detect activated cytolytic lymphocytes. In longitudinal studies, those patients who had cytolytic activity of BAL fluid lymphocytes (range, 8 to 35 percent, n = 4) showed significant improvement in pulmonary function (mean increase in diffusing capacity, 30 +/- 2 percent) in association with decreased BAL fluid cytolytic lymphocyte activity after prednisone treatment. In contrast, patients who initially lacked cytolytic activity in BAL fluid (n = 6) did not improve with prednisone. Activated cytolytic lymphocytes were not observed in the BAL fluid of healthy subjects. These investigations suggest a causal relationship between activated cytolytic lymphocytes in the lung and disease activity in IPF and that assays of activated cytolytic lymphocytes are helpful in identifying patients who will improve with immunosuppressive therapy.
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PMID:Association of activated cytolytic lung lymphocytes with response to prednisone therapy in patients with idiopathic pulmonary fibrosis. 279 74

Peripheral blood T lymphocytes from patients with idiopathic pulmonary fibrosis and matched normal controls were examined for their helper function in an in vitro antibody synthesis assay. This assay measures the dose-related T-cell regulation of antibody production by B cells in the presence of pokeweed mitogen. Eight patients of 14 expressed significantly increased helper T-cell activity, three exhibited no change, and three had depressed helper T-cell function. All of the patients with excessive helper T-cell function had an active neutrophilic alveolitis as determined by bronchoalveolar lavage on the day of study. Five of the 14 patients studied were determined to have a low percentage of neutrophils (less than 10%) in their BAL fluid. None of these were found to express excessive helper T-cell function; in fact three of the five had depressed helper T-cell function. No correlation between steroid therapy or smoking history and the expression of excessive helper function was observed. None of the peripheral blood T-cells from IPF patients were actively producing IL-2 in vitro without further stimulation, providing evidence against constitutive production in vivo. T cells were also examined for their ability to produce lymphokines promoting fibroblast proliferation. Enhanced stimulation of fibroblast proliferation was shown to positively correlate with disease activity as determined by the degree of neutrophilic alveolitis (r = 0.68). The significant correlation between neutrophilic alveolitis and excessive helper T-cell function observed here suggests that altered systemic immunoregulation accompanies local inflammation. The further participation of patient T cells in promoting fibroblast proliferation may contribute to the development of fibrosis, or to the contrary may be an attempt to limit the fibrotic process.
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PMID:Excessive helper T-cell function in patients with idiopathic pulmonary fibrosis: correlation with disease activity. 288 57

Carborundum is a synthetic abrasive manufactured through fusion of high grade silica sand and finely ground carbon in an electric furnace at 2,400 degrees C. It had been considered an inert dust until recently. Two recent epidemiologic studies in Quebec have documented an excess of interstitial lung disease in plant workers and some 30 workers have received workman compensation. Histopathologic lesions have been described in four of the workers. To further investigate the carborundum pneumoconiosis, nine groups of eight sheep were exposed once in the tracheal lobe to either 100 ml saline, 100 mg latex beads in 100 ml saline, 100 mg graphite in 100 ml saline, 100 mg carborundum particles in 100 ml saline, 100 mg ashed carborundum particles in 100 ml saline, 100 mg of quartz (Minusil-5) in 100 ml saline, 100 mg crocidolite fibers in 100 ml saline, 100 mg carborundum fibers in 100 ml saline, and 100 mg ashed carborundum fibers in 100 ml saline solutions. The animals had BAL at two-month intervals and autopsy at month 8. The BAL analyses of cellularity, cytotoxicity and fibrogenicity, in association to necropsy histopathology, documented that all particles except for quartz were inert. The two-carborundum fiber samples produced a similar sustained nodular fibrosing alveolitis and crocidolite asbestos fibers produced a peribronchiolar fibrosing alveolitis of comparable severity. Thus, the major bioactive dusts in the carborundum manufacturing process are quartz particles and the carborundum fibers generated in the process. The latter have fibrogenic activities comparable to asbestos fibers of similar size and are likely to contribute to the pathogenesis of the interstitial lung disease of carborundum workers.
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PMID:Carborundum pneumoconiosis. Fibers in the mineral activate macrophages to produce fibroblast growth factors and sustain the chronic inflammatory disease. 292 13

Angiotensin converting enzyme (ACE) is present in the endothelial cells of the normal lung where it converts angiotensin I to angiotensin II and inactivates bradykinin. It has been suggested that during endothelial injury ACE is sloughed into the blood, and that if the alveolar capillary membrane is injured, also into the alveolar lining fluid. Seven patients with adult respiratory distress syndrome (ARDS), were compared to 11 normal control subjects, nine patients with sarcoidosis, and six with idiopathic pulmonary fibrosis. Total, differential cell counts and ACE determinations were performed on bronchoalveolar lavage fluid in the ARDS group. ACE was detectable in the BAL of all but one ARDS patient. It was concluded that BAL ACE is elevated in some ARDS patients, especially those with infectious causes of lung injury. Increased ACE may reflect endothelial damage or local increase in ACE production in response to sepsis.
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PMID:Angiotensin converting enzyme in bronchoalveolar lavage in ARDS. 302 28

In formulating a reasonable position about the clinical use of BAL and its analysis, one must acknowledge that it is still an experimental procedure that needs further assessment, and it must continue to be included as part of patient research protocols. Therefore, neither the patient nor his/her insurance carrier should foot the bill, yet. The cost involved in analysis of BAL fluid and serum raises another consideration about how many things need to be measured and what tests give the essential information and are the most discriminating. Clearly, all of the assays suggested by some of the BAL results given in table 2 are not necessary. The cell count and the differential count, indicating the relative percentage of lymphocytes among the respiratory cells, and monoclonal antibody staining to distinguish the various T-cell subtypes give most of the essential cell information that relates to activity of alveolitis and to diagnosis in the interstitial lung diseases. Finding a very high percentage of lymphocytes in BAL fluid shifts the differential diagnosis in an unknown diffuse interstitial lung disease to the possibility of a granulomatous process, especially sarcoidosis or hypersensitivity pneumonitis; whereas elevated PMN with about 3% eosinophils also present suggests possible idiopathic pulmonary fibrosis. Many of the protein and enzyme assays have a role in describing immunopathogenesis, but are rarely measured until a few days after the procedure. Some quite sophisticated cell mediators can be measured, such as interleukin-2 produced by helper T-lymphocytes and many macrophage effector substances that may give more precise information than just cell counts and various immunoglobulin values. These assays require complex biochemical and cell culture work and are only available in special research laboratories, limiting the availability of such tests. Thus, it is not easy to suggest just what tests should be conducted with BAL cells and fluid to tailor costs yet give comprehensive clinical information, too. The use of BAL to obtain cells and proteins lining the alveolar space in many ways is still in its infancy, and new applications are being sought for a substantial list of lung diseases. Just the tip of the iceberg has been investigated, and much more may remain to be uncovered.
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PMID:Bronchoalveolar lavage. 354 17

Alveolar hyperventilation is a characteristic feature of the interstitial lung diseases, yet its pathogenesis remains unknown. We examined the relationship between inflammatory alveolar acinar cell counts and the steady state, resting arterial PCO2 in patients with fibrosing alveolitis. To eliminate the influence of overwhelming mechanical lung restriction or resting hypoxemia, we studied 20 patients who, despite having clinicopathologically confirmed fibrosing alveolitis, had vital capacities exceeding 50 percent of predicted, and arterial O2 saturations above 90 percent. There was a significant inverse relationship between the proportion of polymorphonuclear leukocytes (PMNs) in the recovered BAL fluid and the arterial PCO2 (r = -0.67; p less than 0.01). When PCO2 was above 35 mm Hg, the BAL PMN count was 8 percent or less (mean = 3.4; SD = 2.5), while the mean BAL PMN count among those patients whose PCO2 was less than 35 mm Hg was significantly higher (mean = 11.7; SD = 3.7; p less than 0.01). PCO2 levels were unrelated to arterial O2 saturation or PaO2. No relationship was found between the PCO2 and BAL lymphocyte counts. The findings suggest that in fibrosing alveolitis, the arterial PCO2 may be used as an indicator of the state of the inflammatory component of the alveolitis.
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PMID:Arterial PCO2 as an index of activity in fibrosing alveolitis. 681 39

CD14 is a myeloid differentiation antigen which exists in a membrane-bound (55 kD) and a soluble (48 kD) form. This antigen is a receptor for lipopolysaccharide (LPS) structures and triggers the production of various cytokines. The aim of this study was to evaluate whether in active sarcoidosis, a disease with increased proportions of alveolar macrophages (AM) with CD14 expression in BAL fluid, the soluble form of CD14 (sCD14) is also increased. The sCD14 levels were measured in BAL fluid with an ELISA, and membrane-bound CD14 was determined by an immunoperoxidase assay, in active sarcoidosis (n = 13), inactive sarcoidosis (n = 9), idiopathic pulmonary fibrosis (IPF) (n = 6), and control subjects (n = 8). Higher concentrations of sCD14 were present in BAL fluid of patients with active sarcoidosis (58 +/- 34 ng/ml) than in those with inactive disease (13 +/- 10 ng/ml), patients with IPF (5 +/- 5 ng/ml), or control subjects (10 +/- 8% ng/ml) (p < 0.01). Similarly, the proportions of AM expressing membrane-bound CD14 were increased in active sarcoidosis (91 +/- 6%) compared with inactive sarcoidosis (82 +/- 6%), patients with IPF (76 +/- 13%), and control subjects (79 +/- 9%) (p < .05). In sarcoidosis, a significant correlation was found between the sCD14 concentration in BAL fluid and AM membrane expression of CD14 (r = 0.57, p < 0.01). We conclude that sCD14 is increased in BAL of active sarcoidosis suggesting a potential role for this substance as marker of activity and in the pathogenesis of pulmonary sarcoidosis.
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PMID:Soluble CD14 is increased in bronchoalveolar lavage of active sarcoidosis and correlates with alveolar macrophage membrane-bound CD14. 753 Oct 99

Fibrosing alveolitis may occur alone (CFA) or in association with systemic sclerosis (FASSc). FASSc was recently shown to have a prognostic advantage over CFA. Because interleukin-8 (IL-8) is likely to be a major determinant of neutrophil alveolitis, we evaluated IL-8 expression in patients with CFA and FASSc and compared it with that in normal individuals and sarcoidosis and systemic sclerosis patients without pulmonary involvement (SSc no FA). IL-8 protein in bronchoalveolar lavage fluid (BALF) was assessed by immunoassay, and IL-8 mRNA expression was assessed using Northern analysis and reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization of lung parenchyma. Compared with normal subjects, IL-8 concentration was significantly greater in both CFA (p < 0.001) and FASSc groups (p < 0.05) but no different in sarcoidosis. The IL-8 concentration in CFA was higher than in FASSc (p < 0.01) and was related to BAL % neutrophils (rs = 0.48, p < 0.01). IL-8 mRNA expression evaluated by Northern analysis was seen only in patients with CFA and FASSc and was related to BAL % neutrophils (rs = 0.63, p < 0.01). We suggest that IL-8 is a key factor in the pathogenesis of fibrosing alveolitis and that the poorer prognosis of CFA compared with FASSc is related to higher levels of IL-8 within the lower respiratory tract.
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PMID:Interleukin-8. Differential expression in lone fibrosing alveolitis and systemic sclerosis. 773 20

Fibrosing alveolitis (FA) is a common and often fatal complication of systemic sclerosis (SSC). The purpose of this study was to characterize the fibrotic process within the lungs using bronchoalveolar lavage fluid (BALF). We investigated 25 healthy controls (CON) and 85 SSC patients. In 61 patients (72%) lung function tests, clinical, and radiological findings indicated manifest FA, whereas 24 patients (28%) where free of significant lung disease. Of the latter, 12 had pathologic BAL differential cell counts (= subclinical alveolitis; SUB), 12 had normal BAL cytology (NOR). BAL samples were analysed for chemoattractant activity (CAA) for fibroblasts using Boyden chambers. Procollagen-III-Peptide (P-III-P) and Laminin fragment P1 (Lam-P1) were measured radioimmunologically. CAA (expressed as % of the effect of conditioned medium) was increased in FA and SUB (CON: 17.3 +/- 3.2; FA: 40.8 +/- 5.8, p < 0.01 vs. CON; SUB: 58.6 +/- 11.8, p < 0.01 vs. CON; NOR: 23.7 +/- 6.3; n.s.). Lam-P1 [U/ml ELF] was also elevated in FA and SUB patients (CON: 0.90 +/- 0.17; FA: 2.07 +/- 0.48, p < 0.05 vs. CON; SUB: 2.61 +/- 1.14, p < 0.05 vs. CON; NOR: 1.05 +/- 0.35, n.s. vs. CON). P-III-P [U/ml ELF] was elevated in FA patients (CON: 8.3 +/- 1.1; FA: 26.9 +/- 5.5, p < 0.001 vs. CON) but not in SUB or NOR (SUB: 10.2 +/- 0.7, NOR: 7.9 +/- 2.9; n.s.). There was no significant relationship between P-III-P and LAM-P1 values in ELF and serum, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pulmonary manifestations of systemic scleroderma: pathophysiologic and clinical significance of the activation of lung fibroblasts]. 779 85


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