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

Actinobacillus actinomycetemcomitans (AA), is a cocobacillus thin and small, non motile, uncapsulate and capnophilic. AA, is: one of the species encountered in the mouth's comensal flora being able to be isolated in gingival crevices culture and oral mucosa in a 20% of the healthy population. An important number of pathogenic factors make it well equipped, to protect itself from host's defense mechanisms, and to destroy the periodontal tissue. Between the most important we find lipopolisacarides and leucotoxines which promote tisular invasion and destructive qualities of this microorganism. Since 1912, there are numerous reports of infectious process associated to it, between which we find: endocarditis in native and prothesic valve, soft tissues abscess, pneumonia, brain's abscess, urethritis, vertebral osteomielitis, thyroid's abscess, pericarditis and periodontal juvenile illness, being this one in which its isolation is more frequent. In vitro, AA is very susceptible to tetracicline. This antibiotic reaches high concentrations in gingival crevices, has significant affinity to the alveolar bone and contributes to protect the collagen. These special feature make them the election drug in periodontal disease produced by this microorganism.
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PMID:[Role of Actinobacillus actinomycetemcomitans in human infection]. 221 24

Type III procollagen peptide (PCP) is a byproduct of type III collagen synthesis and a potential marker of collagen secretion. In chronic diffuse interstitial lung diseases, elevated PCP concentrations have been found in serum as well as in bronchoalveolar lavage fluid. It has been proposed that PCP is a marker of early, active stages of fibrosis. As severe fibrosis is a frequent complication in adult respiratory distress syndrome (ARDS), we investigated PCP in patients with ARDS and compared the results with those from patients requiring mechanical ventilation because of heart failure and after neurosurgical and surgical interventions, and those from spontaneously breathing patients, including healthy volunteers and patients with pneumonia, liver cirrhosis, and renal failure. PCP concentrations in patients with ARDS were extremely elevated compared with those in control subjects (p less than 0.001) and correlated positively with FiO2 (r = 0.71, p less than 0.01). These results support the pathophysiologic concept of early fibrogenesis in ARDS. As preventing pulmonary fibrosis in ARDS is essential in improving survival rate, we believe PCP can be a valuable diagnostic tool in ARDS.
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PMID:Determination of serum concentrations of type III procollagen peptide in mechanically ventilated patients. Pronounced augmented concentrations in the adult respiratory distress syndrome. 224 Aug 30

We retrospectively prepared step sections of the transbronchial lung biopsy (TBLB) materials which revealed nondiagnostic findings in their original sections in patients with diffuse lung disease, and evaluated the significance of the examination of step sections in the diagnosis of diffuse lung disease. Of 131 cases with nondiagnostic TBLB findings, the preparation of step sections resulted in specific findings in 6 cases (malignancy 3 cases, tuberculosis 1 case, cryptococcosis 1 case and viral infection 1 case), and histopathological changes consistent with the clinical diagnosis in 25 cases. The step section preparation was especially useful for the detection of epithelioid granuloma and tumor tissue in patients with sarcoidosis and carcinoma, respectively, while its contribution to the diagnosis of collagen-vascular disease, hypersensitivity pneumonitis, atypical pneumonia and pneumoconiosis was relatively small. The step section preparation was also useful for the detection of bronchiolitis obliterans. In addition, step sections uncovered clinically unnoticed infection (purulent exudate in the alveolar space) in 6 cases, 3 of whom actually developed pneumonia thereafter. Thus, the preparation of step sections was considered to be useful clinically in 37 cases (28.2%). The preparation of step sections is recommended before a further diagnostic procedure is chosen, when TBLB performed in patients with diffuse lung disease reveals nondiagnostic findings.
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PMID:[Step section preparation of transbronchial lung biopsy material in diffuse lung disease]. 229 Feb 27

Humoral immunity, body reactivity, reparative function of connective tissue were investigated in 45 patients with poor-symptom acute pneumonia and in 29 lingering pneumonia cases. The patients were examined for the content of IgM, IgG and IgA, haptoglobin, seromucoid, collagen metabolism (by oxyproline) on treatment days 1-5 and 15-25. With prolongation of the inflammation resolution and transformation of the disease into a lingering form, there appeared an imbalance of immunoglobulins manifested by low values of IgG and IgA. The latter immunoglobulins being the most active in body defences, this reflects disturbances in the mechanism of humoral immunity responsible for antiinfectious activity. Haptoglobin concentrations were of certain diagnostic significance, its level being higher in lingering pneumonia. In addition, oxyproline (total and bound) level rose thus evidencing catabolism predominance over collagen synthesis. This may underline delayed repair of the connective tissue in the lungs. Seromucoid, on the contrary, proved an unreliable sign. It is concluded that the level of immunoglobulins (IgG and IgA, in particular) as well as high blood haptoglobin and oxyproline with its components can be considered risk factors for poor-symptom pneumonia progression into a lingering one.
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PMID:[Various indicators of early diagnosis of the protracted course of acute pneumonia]. 233 50

Oxidant exposure following chemically induced lung injury exacerbates the tendency to develop pulmonary fibrosis. Influenza virus pneumonitis causes severe acute lung damage that, upon resolution, is followed by a persistent alveolitis and parenchymal changes characterized by patchy interstitial pneumonia and collagen deposition in the affected areas. To determine whether oxidant exposure exacerbates the virus-induced alveolitis and residual lung damage, mice were infected by aerosol inhalation with influenza A virus and continuously exposed to 0.5 ppm ozone or ambient air. Noninfected control mice were exposed to either ambient air or ozone. On various days during the first month after infection, groups of mice were sacrificed and their lungs assessed for acute injury (lung lavage albumin, total and differential cell counts, wet/dry ratios, and morphometry). At 30, 60, 90, and 120 days after infection, groups of mice were sacrificed for total and differential lavage cell counts, lung hydroxyproline content, and morphometric analysis. Ozone exposure did not alter the proliferation of virus in the lungs as quantitated by infectious virus titers of lung homogenates at 1, 4, 7, 10, and 15 days after virus infection but mitigated the virus-induced acute lung injury by approximately 50%. After Day 30 a shift in the character of the pulmonary lesions was observed in that continuous exposure to ozone potentiated the postinfluenzal alveolitis and structural changes in the lung parenchyma. Additional studies suggest that the mechanism for the enhanced postinfluenzal lung damage may be related to the oxidant impairing the repair process of the acute influenzal lung damage. These data demonstrate that ozone exposure mitigates acute virus-induced lung injury and potentiates residual lung damage.
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PMID:Influenza virus infection, ozone exposure, and fibrogenesis. 233 49

To investigate the NMR relaxation times for irradiated rat lung tissue, we measured T1 and T2 at 11 different times during the injury's 1-year time course. A biexponential analysis of T2 was used to determine T2 fast (T2f) and T2 slow (T2s). In addition, we measured water content and correlated changes in the relaxation times with pathological changes. The correlation indicates the following: (1) Shortly after irradiation, the biexponential T2 decay for 1/3 of the samples became monoexponential and there were no noticeable pathological changes observed using light microscopy. (2) During radiation pneumonitis, T2f and T2s were prolonged. This accompanied acute edematous changes and inflammatory cell infiltration. (3) Finally, during radiation fibrosis T1 shortened and collagen increased. We observed no significant correlation between relaxation time changes and water content changes throughout the 1-year time course.
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PMID:A 1-year time course study of the relaxation times and histology for irradiated rat lungs. 234 15

Idiopathic bronchiolitis obliterans-organizing pneumonia (BOOP) is characterized by air space fibrosis of unknown origin. Clinical resolution under steroid treatment suggests the removal of the fibrotic lesion. Open lung biopsies of four patients with idiopathic BOOP were studied by immunochemistry and electron microscopy. Three distinct cell-matrix patterns of intra-alveolar bud were found to represent the sequential evolution of the fibrotic process: fibrinoid inflammatory cell clusters in which immunoglobulins and procoagulant factors (fibrinogen, factors VII and X) were identified; fibroinflammatory buds in which desmin-containing fibroblasts were observed migrating, proliferating, and secreting matrix proteins; fibrotic buds in which myofibroblasts organized a loose connective matrix predominantly composed of fibronectin and type III collagen. Extending forms of fibrotic buds may join contiguous alveoli. Fibrotic bud remodeling ability is correlated to the nature and organization of the matrix components but the factors permitting intra-alveolar matrix degradation must be characterized.
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PMID:Intra-alveolar fibrosis of idiopathic bronchiolitis obliterans-organizing pneumonia. Cell-matrix patterns. 237 39

Bleomycin is a commonly used antineoplastic agent which produces dose- and time-dependent pneumonitis and fibrosis in humans. The mechanism of bleomycin-induced lung injury is uncertain. However, current data shows that bleomycin can generate reactive oxygen species such as superoxide and hydroxyl radicals. We therefore investigated whether intraperitoneal (i.p.) injection of endotoxin, a protectant for hyperoxia, could modulate the biochemical and morphological estimates of bleomycin-induced lung fibrosis in rats. However, pretreatment with multiple i.p. injections of endotoxin, combined with intratracheal bleomycin instillation, resulted in increased lung collagen content compared to bleomycin treatment alone and controls. Furthermore, morphological estimates of the severity of lung lesions present in the endotoxin-bleomycin treatment group were increased when compared with saline and endotoxin control lung lesions. These data indicate, in the current study design, that endotoxin did not reduce, but instead increased the severity of bleomycin-induced pulmonary fibrosis in rats. The mechanism for this increase in fibrosis may be the result of pre-existing endotoxin-induced cell injury.
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PMID:The effect of endotoxin on bleomycin-induced lung fibrosis in the rat. 241 66

It has been proposed that the pneumonitis and subsequent lung fibrosis induced by bleomycin occurs when bleomycin is complexed with ferrous iron and oxygen. In order to see whether chelation of free iron reduced tissue damage induced by intratracheal bleomycin, deferoxamine (DFO) was administered by continuous subcutaneous infusion to overcome its rapid renal excretion. Thirty-three rats received DFO and 30 rats received an equivalent volume of saline by 7-day infusion pumps. Three days after commencement of infusion, half of each group received intratracheal bleomycin, the remainder received intratracheal saline. Three weeks after intratracheal injection, the rats were killed and their lungs were removed for histologic and morphometric assessment and collagen estimation. When compared with animals given intratracheal saline, both bleomycin-treated groups had significant evidence of lung toxicity, but DFO was not protective. Similarly, DFO infusion did not reduce the elevation in collagen concentration (bleomycin/saline, 49 +/- 3.6; bleomycin/DFO, 49.8 +/- 4.1; saline/saline, 39.6 +/- 3.9; saline/DFO, 43.4 +/- 3.8 mg.g-1 wet lung weight) or total lung collagen (bleomycin/saline, 29.9 +/- 6.3; bleomycin/DFO, 33.7 +/- 1.8; saline/saline, 15.5 +/- 2.2; saline/DFO, 17.8 +/- 1.9 mg.left lung-1) induced by bleomycin. This lack of effect was not due to iron contamination of the DFO in the pump or to loss of chelation capacity of DFO, at least for as long as 6 days after pump implantation. No DFO was detected in homogenized lung tissue (limits of detection of assay was 8 x 10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deferoxamine infusion does not inhibit bleomycin-induced lung damage in the rat. 246 74

Bleomycin is a commonly used antineoplastic compound that can produce a dose- and time-dependent pneumonitis and fibrosis in humans. The mechanism of bleomycin-induced fibrosis is not known. However, current data suggest that the production of oxygen radicals by way of a ferrous ion-molecular oxygen mechanism might be related to the pulmonary fibrosis. Therefore, we evaluated the possibility that parenterally administered deferoxamine, an iron chelating compound, could modulate the morphologic and biochemical estimates of bleomycin-induced lung fibrosis in hamsters. Deferoxamine pretreatment and daily injection for 21 days after intratracheally administered bleomycin resulted in a 33% reduction in lung collagen accumulation compared with that after bleomycin treatment alone. However, fibrosis was still present in the bleomycin-deferoxamine group; the animals showed a 142 and 150% increase in lung collagen compared with that in saline- and deferoxamine-treated control animals, respectively. Morphologic estimates of the severity of fibrosis in the bleomycin-deferoxamine treatment group were reduced when compared with the bleomycin treatment group alone, but was increased compared with saline- and saline-deferoxamine-treated control animals. These data indicate that deferoxamine treatment reduces the severity of bleomycin-induced pulmonary fibrosis in hamsters. The mechanism might be by the prevention of iron-catalyzed, free-radical formation.
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PMID:The effect of deferoxamine on bleomycin-induced lung fibrosis in the hamster. 258 89


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