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)

Alveolar and lower respiratory tract immunity in addition to systemic immunity in 31 patients with pleural plaques found on chest X-rays were evaluated. All cases had occupational histories of asbestos exposure, but ferruginous bodies in BAL fluid were only detected in 21 of 31 cases. The percentage of cell components in BAL fluid was evaluated according to the number of ferruginous bodies found in the BAL fluid. As the number of ferruginous bodies increased, neutrophils and T lymphocytes decreased, but B lymphocytes increased. Furthermore, CD25-positive cells were remarkably increased in patients with high exposure to asbestos. In addition, CD25-positive cells in the peripheral blood and serum soluble IL-2 receptors were elevated in the patients with high exposure to asbestos.
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PMID:[Evaluation of immunity based on bronchoalveolar lavage fluid in patients with pleural plaque in the chest X-ray]. 175 18

In 10 patients who received a heart lung transplant, TNF-alpha generation by cells collected during bronchioloalveolar lavages (n = 30) and by circulating mononuclear cells was measured. Basal and recombinant IL-2-stimulated productions (50 U/ml) were measured. TNF-alpha concentration was determined by an immunoradiometric assay (IRMA). Circulating mononuclear cells produced at least 4 times less TNF-alpha than BAL cells. Rejection episodes or CMV diseases were not associated with significant changes in TNF-alpha generation. Recombinant IL-2 increased this production in both cell populations but the magnitude of this effect was smaller in BAL cells, suggesting an in vivo preactivation.
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PMID:[TNF-alpha synthesis by cells from bronchioloalveolar lavage and by circulating mononuclear cells in recipients of heart-lung transplantation]. 183 12

In 7 patients with pulmonary alveolar proteinosis, differential cytology and lymphocyte subsets in BAL fluid were investigated. The study showed that pulmonary alveolar proteinosis is another disorder characterized by a lymphocytic alveolitis and activation of T-lymphocytes (expression of HLA-DR antigens and IL-2 receptors). Our data indicate that immunological mechanisms involving T-cell activation may contribute to be pathogenesis of pulmonary alveolar proteinosis.
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PMID:[Detection of the activation of alveolar lymphocytes in alveolar proteinosis]. 236 99

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

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

Cells from recovered BAL fluid and from infiltrates in different involved tissues (lungs, lymph nodes, conjunctiva, liver, spleen, and skin) were studied in 22 patients with active sarcoidosis in order to define the surface phenotype, functional in vitro properties, and topographic distribution of the cells in granulomatous lesions. Our data demonstrated a compartmentalization of activated T cells with immunoregulatory functions from the blood to all sites of disease activity. In fact, these cells were found to express the T4+ Leu 8- 5/9+ T17- phenotype, which belongs to cells with helper activity, and that provide heightened responses in functional assays of helper activity, IL-2 release, and the ability to respond in AMLR's. Both a cellular redistribution and a local in vitro replication account for this tissue compartmentalization in sarcoidosis. The microanatomic location of activated T cells, as defined by immunohistological evaluation, showed that the state of activation in these T cells may be a consequence of an intimate contact between helper cells and macrophages within the sarcoidosis granulomas.
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PMID:Activated T cells with immunoregulatory functions at different sites of involvement in sarcoidosis. Phenotypic and functional evaluations. 294 79

T cell-replacing factor (TRF)/IL-5 is a glycosylated polypeptide that acts as a key factor for B cell growth and differentiation. Since IL-5 action is probably mediated by specific cell surface receptor(s), we have characterized the binding of IL-5 to cells using biosynthetically [35S]methionine-labeled IL-5 and 125I-IL-5 that had been prepared using Bolton-Hunter reagent. The radiolabeled IL-5 binds specifically to BCL1-B20 (in vitro line) (a murine chronic B cell leukemic cell line previously shown to differentiate into IgM-secreting cells in response to IL-5) within 10 min at 37 degrees C. There are two classes of binding sites with high affinity (Kd = 66 pM) and low affinity (Kd = 12 nM) for IL-5 and an average number of binding sites for high affinity and for low affinity were 400 and 7,500 per cell, respectively. The specificity of binding of radiolabeled IL-5 has been confirmed by demonstrating that only unlabeled IL-5 and anti-IL-5 mAb but not by IL-1, IL-2, IL-3, IFN-gamma, and GM-CSF inhibit radiolabeled IL-5 binding to BCL1-B20 cells. Treatment of surface-bound radiolabeled IL-5 with bivalent crosslinkers identified a membrane polypeptide of Mr 46,500 to which IL-5 is crosslinked. A variety of cell types have been surveyed for the capacity to bind specifically radiolabeled IL-5 with high affinity. BCL1 cells MOPC104E (murine myeloma cell line) expressed IL-5-R, whereas BAL. 17 and L10 A (B cell lymphoma) did not. T cell line, mastocytoma cell line, or macrophage tumor cell line did not display detectable levels of IL-5-R. were hardly detectable on normal resting B cells but were expressed on LPS-activated B cells, fitting the function of IL-5 that acts on activated B cells for their differentiation into Ig-secreting cells. Intriguingly, early B cell lines (J-87 and T-88) that grow in the presence of IL-5 expressed significant but low numbers of high-affinity binding sites for IL-5. The biological effects of IL-5 were mediated by high-affinity binding sites. The identification and characterization of IL-5-R should provide new insight into the apparent diverse biological activities of IL-5.
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PMID:Receptors for T cell-replacing factor/interleukin 5. Specificity, quantitation, and its implication. 326 7

Increasing evidence suggests a role for activated T cells and cytokines in the regulation of eosinophilic inflammation in asthma. In this study, we investigated the distribution of leukocytes, lymphocytes, their activation state, and the cytokine profile in BAL from 10 atopic asthmatics with positive skin prick tests and elevated specific IgE levels to birch or grass pollen. Using segmental allergen challenge, 250 PNU of the appropriate allergen or saline were instilled into different segments, which were lavaged 10 min (10 min) and 18 h (18 h) after allergen challenge or 18 h after saline challenge (C). In peripheral blood the number of neutrophils and activated IL-2R+/CD4+ T cells increased significantly 18 h after allergen provocation; there was no change in eosinophils, other leukocytes, or lymphocyte subsets. In contrast, numbers of eosinophils, neutrophils, and IL-2R+/CD4+ T cells increased significantly in BAL samples at 18 h. The numbers of neutrophils and eosinophils were not significantly different in the lavage performed at 10 min and at C. Analysis of cytokines in concentrated BAL fluid revealed significantly increased levels of IL-5, IL-2, IL-1, TNF-alpha, IL-6, IL-8, and GM-CSF, but not of IL-4 and IFN-gamma at 18 h compared with those at C and at 10 min. The correlation between IL-5 levels, eosinophil numbers, and activated T cells supports a role for T-cell-derived IL-5 in causing tissue eosinophilia in allergic asthma.
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PMID:T cells and cytokines in bronchoalveolar lavage fluid after segmental allergen provocation in atopic asthma. 769 73

T-lymphocyte (T-LC)-derived cytokines have been implicated in asthma pathogenesis. Activation of peripheral blood CD4 but not CD8 T-LC and a Th2-type pattern of elevated cytokine mRNA expression in BAL fluid T-LC have been observed in asthmatics, but the principal source (CD4 or CD8 T-LC) of these cytokines is unknown. Our objective was to measure expression of Th1- and Th2-type cytokine mRNA and spontaneous secretion of IL-3, IL-5, and GM-CSF by peripheral blood CD4 and CD8 T-LC from asthmatics before and after oral glucocorticoid therapy and non-asthmatic controls. We used in situ hybridization to detect mRNA expression in isolated CD4 and CD8 T-LC, and an in vitro eosinophil survival assay to detect secretion of IL-3, IL-5, and GM-CSF in T-LC culture supernatants. Comparing the asthmatics with the controls, elevated percentages of CD4 T-LC expressed mRNA encoding IL-5, IL-4, and GM-CSF (P < 0.02) but not IL-3, IL-2, or IFN-gamma. In CD8 T-LC, mRNA expression was generally low with no significant differences between the groups. In the asthmatics, the percentages of CD4 T-LC expressing IL-5 mRNA correlated with disease severity and the numbers of peripheral blood eosinophils (P < 0.01). Culture supernatants of asthmatic CD4 but not CD8 T-LC exhibited significantly higher (P = 0.0003) eosinophil survival-prolonging activity compared with controls, in which low activity was detected. Inhibition with anti-cytokine antibodies suggested that GM-CSF, and to a lesser extent IL-5 and IL-3, could account for this activity. After oral glucocorticoid therapy of the asthmatics, lung function improved and the percentages of CD4 T-LC expressing mRNA encoding IL-3, IL-5, and GM-CSF but not IL-2, IL-4, or IFN-gamma were reduced (P < 0.04). Secretion of eosinophil survival-prolonging activity by the CD4 T-LC was also reduced (P = 0.004). We conclude that peripheral blood CD4 but not CD8 T-LC from asthmatics express cytokine mRNA in a Th2-type pattern and show elevated secretion of cytokines prolonging eosinophil survival. Glucocorticoid therapy of asthmatics is associated with a reduction in the percentages of CD4 T-LC expressing IL-3, IL-5, and GM-CSF mRNA and secretion of the corresponding proteins.
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PMID:Peripheral blood CD4 but not CD8 t-lymphocytes in patients with exacerbation of asthma transcribe and translate messenger RNA encoding cytokines which prolong eosinophil survival in the context of a Th2-type pattern: effect of glucocorticoid therapy. 774 19

While LCF is present in BAL early after antigen challenge, we know little about its other potential effects beyond CD4+ T cell, monocyte, and eosinophil chemotaxis and monocyte and CD4+ T cell activation. The work described here focuses on the hypothesis that the secreted protein products of T cells participate in the airway inflammatory process that underlies human asthma, and in particular that LCF could play an early role because of the unusual responsiveness of LCF-producing T to histamine. To date, most studies have addressed the measurement of cytokines derived from CD4+ T cells (e.g., IL-2, IL-3, IL-4, IL-5, and GM-CSF) in the airways of asthmatics, and attempted to correlate the presence of protein or mRNA with the complexion of the inflammatory infiltrate. These studies have been based upon the reports that there are increased numbers of CD4+ T cells in the airways of asthmatics, and that the presence of eosinophils might correlate with the secretion of TH2-type cytokines like IL-3, -4, and -5. Using this information as a background, our work has approached the problem in an entirely different way. We have focused our attention on the early events in antigen-induced asthma that are responsible for CD4+ cell accumulation in the lung, including CD4+ T cells, eosinophils, and monocytes. We have attempted to identify mechanisms by which mast cell mediators, in particular histamine, might play a role in the secretion of chemotactic lymphokines that are selective for CD4+ cells by using CD4 itself as a chemotactic factor receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytokine binding to CD4+ inflammatory cells: implications for asthma. 795 94


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