Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pulmonary alveolar macrophage (PAM) is central to lung cellular defenses and is a potential participant in lung injury, but little is known about the influence of the nature and anatomic pattern of acute lung injury on PAM function. To assess the relationship between ongoing pulmonary inflammation and PAM function, we evaluated PAM phagocytic kinetics in a model system of experimental interstitial adjuvant pneumonitis (EIAP) in calves. PAMs were obtained from lung one and seven days postinduction (dpi) of EIAP. Lesions were typical of EIAP, characterized by acute multifocal to coalescing exudative interstitial pneumonitis at 1 dpi, which progressed to granulomatous interstitial pneumonitis by 7 dpi. The total recoverable lung cells and percentage of neutrophils (PMNs) were elevated (P less than 0.01) from animals with EIAP at both 1 and 7 dpi, and there was a four-fold increase (P less than 0.01) in the PAM yield by 7 dpi. Linear regression equations revealed that a larger proportion of control PAMs were phagocytic than were PAMs from animals with EIAP. The mean initial phagocytic rates of PAM following acute lung injury were significantly elevated (P less than 0.05) over controls; this difference was concentration dependent and required a phagocytic bead stimulus concentration in excess of 12.5 x 10(6) beads/ml. PAMs from animals with EIAP had a greater maximum rate of phagocytosis (Vmax) and Km than control PAMs. PAMs from animals with EIAP had a slightly higher proportion of cells which phagocytosed multiple beads. Levels of beta-glucuronidase were elevated (P less than 0.02) in PAM from animals with EIAP at 7 dpi. The results document enhanced PAM phagocytic function in EIAP and differ from our previous experiments in which depressed PAM phagocytic indices were obtained in a model of virus-induced acute bronchiolitis and alveolitis. The functional activities of the PAMs thus appear to be modified by injury-specific events in the lung microenvironment which may, in part, reflect the nature and anatomic pattern of developing pulmonary inflammatory reactions.
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PMID:Influence of acute pulmonary interstitial inflammation on kinetics of phagocytosis by alveolar macrophages. 275 85

The effects of inhaled particulate matter in the workplace and outdoor environment on sensitive subpopulations are not sufficiently investigated in human and animal models. Thus, animal models for pulmonary diseases are necessary for appropriate risk assessment of toxic materials. We studied biochemical characteristics of an acute inflammatory process induced by inhalation of nickel chloride aerosols in rats. Acute bronchiolitis was induced by inhalation of nickel chloride aerosols for 5 days in Wistar rats according to the method described by Kyono et al. (1999). Deterioration and recovery from inflammatory responses were evaluated by analyzing markers of inflammation in bronchoalveolar lavage (BAL) fluid. Experimental animals were sacrificed during and after the nickel aerosol exposure period. The number of neutrophils markedly increased to approximately 0.5 x 10(3) cells/microl BAL fluid during nickel aerosol exposure, accompanied by increase of total protein, soluble L-selectin, cytokine-induced neutrophil chemoattractant/growth-regulated gene products (CINC/GRO), elastolytic activity, trypsin inhibitory capacity, beta-glucuronidase activity, fucose, and sialic acid in BAL fluid compared with those of the control group. There was correlation between number of leukocytes and soluble L-selectin concentration. The number of pulmonary macrophages in BAL fluid decreased to approximately 15% of those of the control group on the days of nickel aerosol exposure. The level of CINC/GRO recovered to that of the control group on day 3 after cessation of the nickel aerosol exposure. However, other inflammatory markers remained at the elevated levels. Changes in the markers of inflammation during and after the nickel aerosol exposure were consistent with previously reported morphological findings. The results indicated that this animal model is potentially useful as an acute bronchiolitis model.
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PMID:Inflammatory responses and mucus secretion in rats with acute bronchiolitis induced by nickel chloride. 1202 13