Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We exposed rats once by nose only for 50 min to a mean concentration of 800 micrograms/m3 of beryllium metal (initial lung burden, 625 micrograms) to characterize the acute toxic effects within the lung. Histological changes within the lung and enzyme changes within bronchoalveolar lavage (BAL) fluid were evaluated at 3, 7, 10, 14, 31, 59, 115, and 171 days postexposure (dpe). Beryllium metal-exposed rats developed acute, necrotizing, hemorrhagic, exudative pneumonitis and intraalveolar fibrosis that peaked at 14 dpe. By 31 dpe, inflammatory lesions were replaced by minimal interstitial and intraalveolar fibrosis. Necrotizing inflammation was observed again at 59 dpe which progressed to chronic-active inflammation by 115 dpe. This inflammation worsened progressively, as did alveolar macrophage and epithelial hyperplasia, becoming severe at 171 dpe. Low numbers of diffusely distributed lymphocytes were also present but they were not associated with granulomas as is observed in beryllium-induced disease in man. Throughout the experiment, total numbers of cells were elevated within the BAL samples due primarily to increased numbers of neutrophils. Lymphocytes were not elevated in BAL samples collected from beryllium-exposed rats at any time after exposure. Lactate dehydrogenase (LDH), beta-glucuronidase, and protein levels were elevated in BAL fluid from 3 through 14 dpe but returned to near normal levels by 31 dpe. LDH increased once again at 59 dpe and remained elevated at 171 dpe. beta-Glucuronidase and protein levels were slightly, but not significantly, elevated from 31 through 171 dpe. Results indicate that inhalation of beryllium metal by rats results in severe, acute chemical pneumonitis that is followed by a quiescent period of minimal inflammation and mild fibrosis. Progressive, chronic-active, fibrosing pneumonitis is observed later. Chronic beryllium lung disease of man is an immunologically mediated granulomatous lung disease, whereas beryllium-induced lung lesions in rats appear to be due to direct chemical toxicity and foreign-body-type reactions.
 ...
PMID:The acute toxicity of inhaled beryllium metal in rats. 208 18

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.
 ...
PMID:Influence of acute pulmonary interstitial inflammation on kinetics of phagocytosis by alveolar macrophages. 275 85

Qualitative and quantitative evaluations of the cellular components of bronchoalveolar washings of calves with experimental parainfluenza-3 virus pneumonitis and control calves were made. Calves were exposed to 10(9) TCID50 of PI-3 by intranasal aerosol exposure and bronchoalveolar cells obtained 7 days after infection by volume-controlled bronchopulmonary lavage. Transient tachypnea and pyrexia occurred in all infected calves, and virus was recoverable at 7 days from nasal swabs and lung tissue. Pulmonary lesions were typical of viral pneumonitis, characterized by patchy alveolitis and bronchiolitis with accumulations of cells and inflammatory debris. The mean total lavage cell yield was elevated in the virus-infected calves, and the percentage of neutrophils was elevated (P less than 0.05). Increased numbers of pulmonary alveolar macrophages (PAM) were also recovered but the difference was not significant. Linear regression equations showed that a decreased proportion of PAM from virus-infected animals were phagocytic. The mean initial phagocytic rates of macrophages from calves with viral pneumonitis were significantly decreased (P less than 0.05) over controls. This difference was concentration dependent and required a phagocytic stimulus in excess of 12.5 X 10(6) beads/ml. Studies of phagocytic kinetics showed that PAM from calves with viral pneumonitis had a lower Vmax than PAM from control calves, but that Km values were comparable. No differences in PAM beta-glucuronidase and acid phosphatase activity were observed. These results indicate depressed phagocytic function in PI-3 virus-inflamed lungs relative to controls. In concert with virus-induced airway lesions, such in vivo depression of PAM phagocytic functions would be expected to depress pulmonary particulate clearance and lung defense mechanisms.
 ...
PMID:Alveolar macrophage phagocytic kinetics following pulmonary parainfluenza-3 virus infection. 303 12

Biochemical and functional measurements of rat pulmonary alveolar macrophages were measured 4 h after 1 10-s, 26 to 28% total body surface area, full-thickness scald burn induced under ether anesthesia. Both phagocytic activity and capacity were significantly decreased to a comparable extent, whereas microbicidal activity was increased almost twofold in macrophages from the burned animals. Concurrent with the decreased phagocytic function was a marked impairment in chemotaxis and random migration of these cells when zymosan-activated serum was used as the chemoattractant. When biochemical parameters were examined, it was demonstrated that, on a per-cell but not total-protein basis, alveolar macrophages from burned animals had elevated levels of RNA, total protein beta-glucuronidase, acid phosphatase, and 5'-nucleotidase. These results raise the possibility that the increased pneumonitis in burned individuals may be due to more complex macrophage dysfunctions than impaired microbicidal activity, as was once thought. Alternatively, the biochemical and functional changes observed may be a reflection of a new population of macrophages appearing in the lungs after thermal injury.
 ...
PMID:Biochemical and functional alterations in macrophages after thermal injury. 620 38

We report a case of chronic myelogenous leukemia (CML) associated with pronounced peripheral lymphadenopathy, with the cells having the philadelphia (Phl) chromosome and T-cell features. A 23-year-old man who was diagnosed as having CML and treated with busulfan was admitted to our hospital because of increasing hepatosplenomegaly and pronounced lymphadenopathy. An axillary lymph node biopsy disclosed that the malignant cells formed rosettes with neuraminidase-treated sheep red blood cells (En) (95.0%) and were positive for Leu 1 (91.8%). Of the cytochemical reactions, peroxidase was negative and periodic acid-Shiff, acid alpha-naphthyl acetate esterase and beta-glucuronidase were all positive. The karyotype of the bone marrow cells was 46 XY Phl positive (22q-), and that of the lymph node cells was 51 XY Phl positive +8, +9, +18, +19, +21, 22q-. He was treated with various anti-leukemic agents and irradiation. Despite such treatments, he died of pneumonia. This is a report of a CML patients with blast crisis and tumor formation characterized by T-cell features.
 ...
PMID:Blast crisis of chronic myelogenous leukemia with tumor formation characterized by T-cell features--a case report. 660 8

To study the in vivo toxicity of respirable particles, bronchoscopic catheterization of the sheep tracheal lobe was used to expose a limited area of the lung. After control studies, 3 groups of 6 sheep received one exposure to either 100 ml saline, 100 mg of latex beads (1.0 mu diam.) in saline or 100 mg of UICC Canadian chrysotile asbestos in saline. The animals were studied at day 1, 8, 15, 22 and 29 by pulmonary function tests (PFT) and bronchoalveolar lavage (BAL). At day 29, the sheep had chest roentgenograms (CR) and were autopsied. In all sheep, PFT did not changed and CR showed minimal infiltrates only in the asbestos-exposed sheep. In the saline sheep, BAL and lung histology did not change. In the latex sheep, at day 1 total BAL cells increased to 370%, macrophages to 215% and neutrophils to 650% (P less than 0.01) without change in BAL proteins or enzymes. These returned to control levels at day 8 and after except for a slight increase in BAL neutrophils. The lung histology showed inflammatory changes without architectural distortion. In the asbestos sheep, the day 1 response was comparable to latex group in terms of BAL cellularity but BAL neutrophils remained significantly elevated at 40% total BAL cells at day 8, 15, 22 and 29. Also lactate dehydrogenase (LDH) and beta-glucuronidase in BAL were significantly elevated from day 1 to day 29. At autopsy, the tracheal lobe of asbestos sheep had pneumonia-like neutrophilic infiltrates in the surroundings of the peripheral airways with early peribronchiolar fibrosis. This new in vivo model can clearly and rapidly differentiate the relative toxicity of respirable particles in the lung tissue and thus should be a useful tool in environmental lung research.
 ...
PMID:Rapid in vivo assessment of toxicity of respirable particles: a concise report. 687 67

Inhaled beryllium (Be) can induce a range of adverse pulmonary responses in animals and humans including acute pneumonitis, chronic granulomatous lung disease, and cancer. To facilitate comparisons with our previous data describing Be toxicity in rats, we evaluated the toxic effects of inhaled Be metal in mice. Groups of 34 strain C3H/HeJ mice were acutely exposed by the nose-only route to aerosolized Be metal to achieve measured initial lung burdens of 0, 1.7, 2.6, 12, or 34 microg. All mice received aerosolized 85 Sr-labeled fused aluminosilicate particles (85 Sr-FAPs) immediately before their Be exposure so that the influence of Be on lung retention of these poorly soluble tracer particles could be externally quantitated. Groups of mice were euthanized at 8, 15, 40, 90, 210, and 350 days after exposure for evaluation of histopathological changes and for cytologic and biochemical indicators of lung damage measured in bronchoalveolar lavage fluid. Clearance of 85 Sr-FAP tracer particles through 196 days after exposure was delayed in mice receiving the 12 and 34 microg Be lung burdens, but not the 1.7 or 2.6 microg lung burdens. Increased total cell numbers, increased percentage of neutrophils, and elevated levels of total protein and the activities of beta-glucuronidase and lactate dehydrogenase in bronchoalveolar lavage fluid were observed in the two highest Be lung burden groups compared with controls. Lung lesions included particle-containing macrophages, granulomatous pneumonia, lymphocytic interstitial aggregates, and mononuclear interstitial infiltrates. These lesions were occasionally seen in mice receiving the 2.6 microg lung burden, were present in most of the mice receiving 12 or 34 microg lung burdens, and were generally increased in severity with time and lung burden. Thus, we have demonstrated that a single, acute inhalation exposure to Be metal can chronically retard particle clearance and induce lung damage in mice. The initial lung burdens used caused responses ranging from no apparent effects to significant Be-induced responses. A comparison of these data with our previous data from rats indicates that the mass of Be metal required to induce lung damage in mice is similar to that needed for rats. When expressed on a lung weight-normalized basis, mice appeared to be more resistant to the toxic effects of inhaled Be than rats.
 ...
PMID:Dose-response relationships between inhaled beryllium metal and lung toxicity in C3H mice. 953 46

The toxicity of 4-ethyltoluene to experimental animals was studied after single and repeated exposures. It was found that 4-ethyltoluene can be classified as a very mild skin and eye irritant. Sensory respiratory irritation of 4-ethyltoluene was studied in Balb/C male mice using the plethysmographic method. The concentration at which the respiratory rate decreased to 50% (RD50 value) was determined to be 4216 mg/m3 (2795-5850 mg/m3 for 95% confidence interval). To study repeated-dose inhalation toxicity, male and female outbred Wistar rats were exposed in a dynamic inhalation chamber to 4-ethyltoluene vapours at concentrations of 477 or 2337 mg/m3, 6 h/day, 5 days/week for 4 weeks (20 exposure days). No significant changes were observed in food consumption and body weight gain. Statistically significant, concentration-dependent changes in the number of total cells, as well as of macrophages, polymorphonuclear leucocytes and lymphocytes were found in bronchoalveolar lavage. In the fluid of bronchoalveolar lavage, a significant, concentration-related increase was noted in total protein and mucoproteins and the activity of beta-glucuronidase, gamma-glutamyl transferase, lactate dehydrogenase and acid phosphatase. Histopathology revealed an increased rate of bronchitis and pneumonia and perivascular lymphoid infiltrations in rats exposed to 2337 mg/m3 of 4-ethyltoluene.
 ...
PMID:Studies on dermal, ocular and respiratory effects of 4-ethyltoluene in experimental animals. 1127 44

A nonphotochromogenic, rapidly growing Mycobacterium strain was isolated in pure culture from the sputum and the bronchoalveolar fluid of a patient with hemoptoic pneumonia by using axenic media and an amoebal coculture system. Both isolates grew in less than 7 days at 24 to 37 degrees C with an optimal growth temperature of 30 degrees C. The isolates exhibited biochemical and antimicrobial susceptibility profiles overlapping those of Mycobacterium abscessus, Mycobacterium chelonae, and Mycobacterium immunogenum, indicating that they belonged to M. chelonae-M. abscessus group. They differed from M. abscessus in beta-galactosidase, beta-N-acetyl-beta-glucosaminidase, and beta-glucuronidase activities and by the lack of nitrate reductase and indole production activities, as well as in their in vitro susceptibilities to minocycline and doxycycline. These isolates and M. abscessus differed from M. chelonae and M. immunogenum by exhibiting gelatinase and tryptophane desaminase activities. Their 16S rRNA genes had complete sequence identity with that of M. abscessus and >99.6% similarity with those of M. chelonae and M. immunogenum. Further molecular investigations showed that partial hsp65 and sodA gene sequences differed from that of M. abscessus by five and three positions over 441 bp, respectively. Partial rpoB and recA gene sequence analyses showed 96 and 98% similarities with M. abscessus, respectively. Similarly, 16S-23S rRNA internal transcribed spacer sequence of the isolates differed from that of M. abscessus by a A-->G substitution at position 60 and a C insertion at position 102. Phenotypic and genotypic features of these two isolates indicated that they were representative of a new mycobacterial species within the M. chelonae-M. abscessus group. Phylogenetic analysis suggested that these isolates were perhaps recently derived from M. abscessus. We propose the name of "Mycobacterium massiliense" for this new species. The type strain has been deposited in the Collection Institut Pasteur as CIP 108297(T) and in Culture Collection of the University of Goteborg, Goteborg, Sweden, as CCUG 48898(T).
 ...
PMID:Amoebal coculture of "Mycobacterium massiliense" sp. nov. from the sputum of a patient with hemoptoic pneumonia. 1558 72