Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify the activation of alveolar macrophages as a direct measure of disease activity in pulmonary sarcoidosis and to evaluate the possible relationship with serum angiotensin-converting enzyme (ACE) levels, we studied the morphology and function of alveolar macrophages obtained by bronchoalveolar lavage from patients with active disease (n = 12) and inactive disease (n = 5), and from normal controls (n = 11). At the time of lavage, 6 of 12 patients with active disease showed an elevation of serum ACE levels. When alveolar macrophages were cultured, more cells from active disease adhered to glass, spread out, and were positive for NBT reduction (p less than 0.001). Lysosomal enzyme (beta-galactosidase) activity was higher only in patients with active disease (p less than 0.001). In active disease, there were no significant differences in morphology or function of alveolar macrophages between higher and normal serum ACE levels. Thus, alveolar macrophages were activated in active pulmonary sarcoidosis and no correlation was found with serum ACE levels. These results suggest that serum ACE levels do not accurately reflect the activity of disease in the lung.
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PMID:Activation of alveolar macrophages in pulmonary sarcoidosis: lack of correlation with serum angiotensin-converting enzyme activity. 301 35

Alveolar macrophages from patients with active pulmonary sarcoidosis have been shown to secrete several factors, such as interleukin-1 and alveolar macrophage-derived growth factor. We examined alveolar macrophages from nonsmoking patients with sarcoidosis undergoing bronchoalveolar lavage (BAL) for evaluation of disease activity. We compared these cells with macrophages from smoking and nonsmoking control patients. The amount of hydrogen peroxide released by the macrophages either spontaneously or after stimulation by phorbol myristate acetate was measured. The alveolar macrophages from smokers spontaneously released hydrogen peroxide, as we previously observed. The macrophages from the patients with sarcoidosis also released detectable amounts of hydrogen peroxide, but the macrophages from the non-smokers did not. Alveolar macrophages from all three groups released hydrogen peroxide when stimulated with phorbol myristate acetate. The macrophages from all three groups were examined for the presence on the surface membrane of beta-galactosidase, an enzyme that appears on the surface of older, activated macrophages. The macrophages in the BAL fluid of the patients with sarcoidosis had less beta-galactosidase staining than did those from the smokers, although they released comparable amounts of hydrogen peroxide. These findings suggest that alveolar macrophages in the BAL fluid of patients with sarcoidosis are younger, more monocyte-like, and activated by various factors, including gamma-interferon.
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PMID:Spontaneous hydrogen peroxide release from alveolar macrophages of patients with active sarcoidosis: comparison with cigarette smokers. 312 8

Adenovirus (Adv)-mediated gene transfer requires efficient infection of target cells. The objective of this study was to establish whether alveolar macrophages (AM) and T cells (AT) from sarcoid patients were permissive to infection with Adv vectors and if this property could be used to investigate cytokine gene regulation. Sarcoid and normal bronchoalveolar lavage (BAL) specimens infected with Adv vectors expressing either beta-galactosidase or a green fluorescent protein were analyzed for transgene expression by fluorescence-activated cell sorter (FACS) and direct immunofluorescence, respectively. Expression of surface antigens previously associated with Adv infection, the coxsackie/adenovirus receptor (CAR), alpha v beta 3, and alpha v beta 5 integrins, was also assessed using FACS analysis. Sarcoid AM and AT were found to efficiently express Adv transgenes, unlike AM from normal volunteers, peripheral blood monocytes, and peripheral blood T cells. Cells permissive to Adv infection expressed the CAR and alpha v beta 5 integrin (also alpha v beta 3 integrin for AM). The data indicate that the upregulation of Adv receptors and the ability to infect sarcoid AM and AT are related to the inflammatory environment within the lung. Having demonstrated efficient Adv-mediated transgene delivery to sarcoid AM and AT, a construct encoding porcine I kappa B alpha was then used to investigate the requirement for nuclear factor (NF)-kappa B in the regulation of cytokine gene expression in pulmonary sarcoidosis. Overexpression of I kappa B alpha in sarcoid BAL specimens indicated that tumor necrosis factor-alpha and interleukin (IL)-6 production by AM and interferon (IFN)-gamma production by AT is NF-kappa B dependent, whereas IL-4 production by AT is NF-kappa B independent. This is the first occasion that the requirement for NF-kappa B in IFN-gamma gene expression within primary human T cells has been demonstrated. The results of this study have implications for the future investigation of molecular pathways in inflammatory lung disease.
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PMID:Alveolar macrophages and T cells from sarcoid, but not normal lung, are permissive to adenovirus infection and allow analysis of NF-kappa b-dependent signaling pathways. 1150 22