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)

We studied the role of macrophages in the process of pulmonary fibrosis, focusing on gene expressions of cytokines. TGF-alpha is a factor which stimulates fibroblasts or endothelial cells to proliferate, by combining to receptors of EGF competitively with EGF in vitro. Total RNA was extracted from alveolar macrophages recovered by bronchoalveolar lavage from patients with idiopathic pulmonary fibrosis or normal healthy volunteers, and the expression of TGF-alpha mRNA was evaluated by Northern analysis. There was no detectable TGF-alpha mRNA in alveolar macrophages from normal healthy volunteers; however, in patients with idiopathic pulmonary fibrosis, a considerable level of mRNA of TGF-alpha could be detected. Using an experimental rat model of alveolitis induced by bleomycin, the expression of TNF-alpha mRNA in alveolar macrophages recovered by BAL was evaluated by Northern analysis. Alveolar macrophages from bleomycin-treated rats expressed a significant level of TNF-alpha mRNA. Both TGF-alpha and TNF-alpha have proliferative activity on fibroblasts, and may have an important role in the process of fibrosis of the lung.
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PMID:[Cytokine gene expression in interstitial lung diseases]. 143 13

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

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

The adult respiratory distress syndrome (ARDS) is a complex syndrome in which pathogenesis is multifactorial. TNF-alpha, known to be pivotal in tissue damage, has been shown to have high levels in blood and alveolar fluid in ARDS. The identification of the cells responsible for this production in the alveolar milieu has not yet been reported. In order to evaluate the TNF-alpha gene expression in ARDS we have analyzed by in situ hybridization, using RNA probes, alveolar macrophages (AM) obtained by BAL from seven patients with ARDS, eight patients with miscellaneous respiratory diseases, and three control patients. In freshly collected AM from patients with ARDS, 66 +/- 14.5% cells expressed the TNF-alpha gene without in vitro stimulation. This TNF-alpha expression does not result from the BAL procedure itself since only a few unstimulated control AM contained TNF-alpha mRNA transcripts. TNF-alpha expression in AM is not restricted to patients with ARDS since it has also been observed in miscellaneous respiratory diseases; however, this expression is a constant feature in ARDS. These results demonstrated the major role of AM in the intra-alveolar production of TNF-alpha, and they point out the necessity in ARDS for a specific intra-alveolar therapy.
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PMID:Expression of tumor necrosis factor-alpha gene in alveolar macrophages from patients with the adult respiratory distress syndrome. 850 72

We used semiquantitative RT-PCR to monitor the expression of mRNA encoding cytokines (IL-1 beta, IL-6, TNF-alpha, and IL-10) and IFN-gamma in fresh isolated peripheral blood mononuclear cells (PBMCs), lymph node mononuclear cells (LNMCs), and mononuclear cells obtained after bronchoalveolar lavages (BALMCs), of four cynomolgus macaques inoculated intravenously with a pathogenic isolate of simian immunodeficiency virus (SIVmac251). To investigate the effects of the viral load on the expression of the cytokines, two monkeys received 30 mg kg-1 day-1 of didanosine (ddI). The two nontreated monkeys became infected and seroconverted, whereas the ddI-treated monkeys were completely protected as demonstrated by all criteria of diagnosis of SIV infection. Concomitant with the peak of viral replication (2 weeks after the experimental inoculation), high levels of IL-6 mRNA were produced in PBMCs, LNMCs, and BALMCs of the two placebotreated infected monkeys. Overexpression of TNF-alpha and IL-10 mRNAs was sometimes observed in LNMCs and BALMCs. A progressive overexpression of IFN-gamma mRNA, starting 2 weeks after experimental inoculation, was observed in BALMCs from infected animals. Concurrently, a marked increase in the CD8+ lymphocyte percentage in the BAL fluids was detected by FACS analysis. Thus, our results emphasize the importance of a comparative study of the expression of cytokines in different tissues. They suggest the interactions of monocyte/macrophage monokine production with viral replication, as well as the role of IFN-gamma in the development of lung cellular immunity to SIV infection.
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PMID:Cytokine mRNA expression in mononuclear cells from different tissues during acute SIVmac251 infection of macaques. 887 Aug 48

Cytokines released from activated alveolar macrophages and T-lymphocytes affect the accumulation of monocyte-macrophage-lineage cells and therefore play an important role in the formation of sarcoid granuloma. Although it is likely that certain monokines and lymphokines are involved in the development of sarcoid granulomas, the evidence for this is not unequivocal. In an attempt to clear critical cytokines in the development and maintenance of sarcoid granuloma, we have measured the level of seven cytokine mRNA (TNF-alpha, IL-6, IL-8, TGF-beta, PDGF-B, IFN-gamma, and GM-CSF) in cells obtained by BAL from sarcoidosis patients and normal subjects. To detect cytokine mRNA, we employed a reverse transcription-polymerase chain reaction. We report that the levels of TNF-alpha, IL-6, PDGF-B and GM-CSF mRNA were significantly increased in BAL cells from the patients with pulmonary sarcoidosis compared to controls. No significant differences were observed in the mRNA expression of IL-8, TGF-beta and IFN-gamma. A significant correlation of the expression of the mRNA levels of seven cytokines in the same patients with sarcoidosis was observed between IL-8 and TNF-alpha, PDGF-B, and IL-6, IL-8 and IL-6 and TFN-alpha and PDGF-B and IL-8. This finding indicates that at least these four cytokines are involved in the cytokine network at the local alveolar site of chronic granulomatous inflammation. This study adds a report to the literature that supports a role for cytokine, TNF-alpha, IL-6, PDGF and GM-CSF in particular, in the promotion and maintenance of sarcoid granulomatous inflammation.
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PMID:Increased expression of tumor necrosis factor-alpha, interleukin-6, platelet-derived growth factor-B and granulocyte-macrophage colony-stimulating factor mRNA in cells of bronchoalveolar lavage fluids from patients with sarcoidosis. 889 83

A nonsmoking 54-yr-old man, employed in a peat moss packaging plant, developed dyspnea and recurrent fever. The diagnosis of hypersensitivity pneumonitis (HP) was made. Thirteen of 14 coworkers and 13 nonexposed control subjects were studied. Five workers were nonsmokers, two were minimal smokers, and six were smokers. HP was found in another subject. Monocillium sp. and Penicillium citreonigrum, 4.6 x 10(7) CFU/g, were found in the peat moss. Three nonsmokers, the two minimal smokers (including the subject with HP), and the index case had antibodies to these microorganisms; none of the six heavy smokers had antibodies. Serum TNF-alpha was higher in the workers than in the control subjects (0.930 +/- 0.177 versus 0. 350 +/- 0.076). Three of the four asymptomatic seropositive workers and two seronegative smokers were further evaluated. All three seropositive workers had normal lung functions and CT but they all had a lymphocytic alveolitis (30, 34, and 68% lymphocytes in their bronchoalveolar lavage [BAL]). The smokers had normal lung functions, CT, and percentage of BAL lymphocytes (3 and 13%). This study identified a previously unrecognized work environment that can lead to HP and documented a protective effect of smoking on the response to antigens.
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PMID:Hypersensitivity pneumonitis in peat moss processing plant workers. 970 Jan 14

Recent observations in asthmatics demonstrated anti-inflammatory and immunomodulatory activities of theophylline besides the bronchodilating effect. Theophylline inhibits the mediator release from mast cells, peripheral blood monocytes and alveolar macrophages. The proliferative response of T-cells as well as the influx of eosinophils in BAL fluid is inhibited by treatment with theophylline. The production and release of pro-inflammatory cytokines are affected by theophylline showing a potent inhibitory effect on the production of IL-1beta, TNF-alpha and IFN-gamma. The production of the anti-inflammatory cytokine IL-10 is increased. Evidence is mounting that the anti-inflammatory effects and immunomodulating actions are exerted at lower plasma concentrations than those required for bronchodilation. These activities are of relevance in the treatment of chronic obstructive pulmonary disease (COPD), a disease in which the inflammatory component is considered to be more important than previously thought.
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PMID:Therapeutic activities of theophylline in chronic obstructive pulmonary disease. 975 87

Azithromycin (AZM) is a new macrolide antibiotic with a high intracellular/extracellular concentration ratio. Immunomodulatory and antiinflammatory properties have been reported with other macrolides, especially erythromycin. The aim of the present study was to evaluate the effect of AZM on the production of proinflammatory mediators by alveolar macrophages (AM) up to 4 weeks after a 3-day course of AZM (500 mg, once a day). Nineteen non-smoking healthy male subjects were investigated with bronchoscopy and bronchoalveolar lavage. Group 1 received no treatment. Groups 2, 3, and 4 were bronchoscoped 1, 7 and 30 days, respectively, after AZM administration. AZM concentrations were simultaneously measured in plasma and in AM extracts. In serum, AZM levels were higher in group 2 (32.8 +/- 14.2 micrograms/l), at the lower limit of detection in group 3 (2.8 +/- 1.7 micrograms/l), and no longer detectable in group 4. In AM extracts, the highest concentrations were measured in group 2 (51.6 +/- 28.3 ng/microliter) and in group 3 (31.8 +/- 17.2 ng/microliter), and were detected up to 30 days after treatment in group 4 (2.9 +/- 2.3 ng/microliter). There was no significant differences between groups for blood or BAL proinflammatory cytokines levels (TNF-alpha, IL-1 beta, IL-6), and for superoxide generation by AM. We conclude that a 3-day course of AZM 500 mg/day in healthy subjects does not alter the proinflammatory cytokine profile in blood and in AM despite the prolonged tissue impregnation by this drug.
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PMID:Function of human alveolar macrophages after a 3-day course of azithromycin in healthy volunteers. 1010 42

An inflammatory cytokine, tumor necrosis factor (TNF)-alpha, has been implicated in the pathogenesis of inflammatory lung diseases such as interstitial pneumonia (IP). To clarify the role of the inflammatory cytokine in the pathogenesis of lung inflammation, we introduced a murine TNF-alpha gene into murine lungs by the hemagglutinating virus of Japan (HVJ)-liposome method. Seven days after the TNF-alpha gene introduction resulted in marked cellular infiltration of alveoli, and mild histological change was observed 28 days after the gene introduction. Electron microscopic analysis revealed minimal deposition of collagen fibrils. Analysis of the BAL revealed that the total cell number was markedly increased 3 and 7 days after the gene introduction, and more than 90% of the cells were macrophages. The increase in the cell number was returned to below the normal level 28 days after the gene introduction. During the development of IP, TNF-alpha may regulate pathologic change of the pulmonary interstitium and alveolar cells.
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PMID:Changes in pulmonary histology and exfoliated bronchoalveolar cells induced by in vivo introduction of the tumor necrosis factor-alpha gene. 1070 60


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