Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbits and rats were infected intratracheally with extracellular enzyme of Streptomyces thermohygroscopicus (H9-4) by only one exposure, and lesions of the lung developed including mononuclear macrophage infiltration as well as bronchitis and vasculitis. The obvious damages in type I pneumocytes, endothelial cells of capillaries and arterioles in the lung were observed by electron microscopy. Immunofluorescent histochemistry examination revealed exudation of plasma fibronectin which might play an important role during the process of lesion repairing in lung. The experiment also confirmed that extracellular enzyme of Streptomyces thermohygroscopicus might directly damage the lung tissue. These experimental data may serve as valuable reference for studying the etiology and pathogenesis of farmer's lung disease.
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PMID:An experimental study of lung lesions caused by extracellular enzyme of Streptomyces thermohygroscopicus. 187 46

Recurrent pulmonary infections with Staphylococcus aureus and Pseudomonas aeruginosa are a major problem in cystic fibrosis (CF), leading to severe and progressive deterioration of the respiratory tract. Fibronectin (FN) has a binding site(s) for S. aureus and Streptococcus pyogenes. This bacterial bindings site(s) was studied by using FN from patients with CF and comparing them with FN purified from the plasma of bronchitis and normal subjects by an enzyme-linked immunosorbent assay technique. We found a decreased binding of the CF FN to these bacteria in all seven CF patients. Other differences between the CF FN and normal FN were a marked modification in the pattern of peptide migration in polyacrylamide gel electrophoresis after hydrolysis with various proteinases and an increase or decrease of the total sugar content of the FN.
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PMID:Modifications of plasma fibronectin in cystic fibrosis patients. 199 40

Rabbits and rats were infected intratracheally with extracellular enzyme of streptomyces thermohygroscopicus (H9-4) for only one exposure and lesions of lung developed which included mononuclear macrophage infiltration as well as bronchitis and vasculitis. The obvious damages in type I pneumocytes, endothelial cells of capillaries and arterioles in the lung were observed by electron microscopy. Immunofluorecent histochemistry examination revealed exudation of plasma fibronectin which might be important to play certein role during the process of wound repairing in lung. The experiment also confirmed that extracellular enzyme of streptomyces thermohygroscopicus might directly damage the lung tissue, and these experimental data may serve valuable reference for studying the etiology and pathogenesis of farmer's lung diseases.
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PMID:[Study of experimental lung lesions caused by extracellular enzyme of Streptomyces thermohygroscopicus]. 258 45

1. Neutrophils from patients with chronic obstructive bronchitis and emphysema or age-matched control subjects were cultured on a substrate of 125I-fibronectin. The neutrophils from patients with lung disease digested significantly more fibronectin and released more elastase into the culture supernatant than did cells from control subjects. Preincubation of neutrophils from emphysematous patients with plasma from control subjects significantly inhibited fibronectin digestion by the patients' neutrophils by, on average, 10%. Preincubation of control subjects' neutrophils with plasma from emphysematous patients had no effect on fibronectin digestion. 2. Tumour necrosis factor increased fibronectin digestion in a dose-dependent manner when the cytokine was added to the adherent cells but not when preincubated with the polymorphonuclear leucocytes in suspension. Bacterial endotoxin in concentrations above 6 micrograms/ml significantly increased fibronectin digestion by neutrophils, but leukotriene B4, interferon-gamma and interleukin-1 alpha had no significant effects. 3. Dexamethasone inhibited fibronectin digestion by neutrophils in a dose-dependent manner, from 11% at 10(-10) mol/l to 68% at 10(-3) mol/l.
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PMID:Effects of plasma, tumour necrosis factor, endotoxin and dexamethasone on extracellular proteolysis by neutrophils from healthy subjects and patients with emphysema. 275 60

Fibronectin/albumin ratios in plasma and in bronchoalveolar lavage fluid were evaluated in patients (1-6 years of age) with recurrent obstructive bronchitis and different interstitial lung diseases. These inflammatory reactions were characterized by increased influx of macrophages on the bronchoalveolar surface, but an increase in the proportion of lymphocytes or neutrophils was also detected in the group of patients with lymphocyte-macrophage or neutrophil-macrophage alveolitis. There was no considerable difference in plasma fibronectin concentrations obtained from healthy children and patients with moderate obstructive bronchitis and slight inflammation of the bronchial mucosa observed bronchoscopically. Levels of plasma fibronectin were elevated in patients with serious bronchial inflammation and different alveolitis, but they were within the normal range. A comparison of lavage fibronectin/albumin ratios with plasma fibronectin/albumin ratios with plasma fibronectin/albumin ratios indicated significant local production of fibronectin in subjects with serious bronchial inflammation and interstitial lung disorders. Fibronectin detected on the bronchoalveolar surface seems to be an important factor in mediating cell-to-cell interactions in the repair of the bronchoalveolar structures, and in tracing the activity of the inflammatory reactions not only in patients with interstitial lung diseases, but also in patients with serious chronic bronchial inflammation.
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PMID:Fibronectin in bronchoalveolar lavage fluid and plasma from children with chronic inflammation of lungs. 320 79

Fibronectin is normally present in the lower respiratory tract. Significantly increased levels of it were detected in the lavage fluid in patients with interstitial lung diseases. Because this molecule appears to mediate a number of components of the inflammatory process, we evaluated the status of fibronectin in plasma and bronchoalveolar lavage in patients with recurrent obstructive bronchitis when signs of severe chronic mucosal inflammation were observed bronchoscopically. There was no considerable difference in plasma concentrations of fibronectin obtained from healthy children and patients. A comparison of lavage fibronectin/albumin ratios with plasma fibronectin/albumin ratios suggested significant local production, especially when the lavage and plasma ratios were measured in the same patients. Phagocytic activity of alveolar macrophages and blood granulocytes from the same patients was enhanced at both concentrations of fibronectin used. This concentrations referred to values quantified in the lavage fluid. The metabolism of fibronectin seems to be an important factor in tracing the inflammation process not only in adults with chronic interstitial lung diseases, but also in children with recurrent obstructive bronchitis.
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PMID:Fibronectin on the bronchoalveolar surface in children with recurrent obstructive bronchitis. 326 64

Toxic effects of SO2 and sulfite such as bronchitis and bronchoconstriction have been well documented. SO2 has also been suggested to potentiate carcinogenic effects of PAH. However, the molecular basis of these toxic effects is unclear. We have examined the covalent reaction of SO2 and sulfite with cellular proteinacious and nonproteinaceous sulfhydryl compounds using rat liver, and lung and human lung derived A549 cells. Reactions of sulfite and protein in rat and human lung cells reveals at least three proteins with sulfite-reactive disulfide bonds. Besides fibronectin and serum albumin, which had been reported to contain sulfonated products following exposure to sulfite, we have found one other protein with sulfite-binding capabilities. Since the integrity of disulfide bonds is crucial to the tertiary structure and thus protein function, the disruption of protein structure by sulfitolysis may result in altered cellular activities leading to biochemical lesions. Using carefully controlled conditions, reproducible GSH contents can be found in cultured cells and used as an experimental basis for studying alterations in the GSH and GSSG content of cells. Sulfitolysis of GSSG results in the formation of GSSO3H in A549 cells, and possibly in the lung. GSSO3H can be reduced enzymatically by GSSG reductase. However, the Km of GSSO3H is high compared to that of GSSG, suggesting the existence of a transient concentration of GSSO3H once it is formed. Cysteine S-sulfonate is, however, not reduced by cytosolic extracts in the presence of NADPH and would have to be eliminated from the cell by other means. GSSO3H is a strong competitive inhibitor of GST in rat liver and lung and A549 cells, using 1-chloro-2,4-dinitrobenzene as a substrate. It also inhibits the formation of GSH conjugates of BP 4,5-oxide, anti and syn BPDE, but to a lesser extent. These results suggest that SO2 may affect the detoxification of xenobiotic compounds by inhibiting, via formation of GSSO3H, the enzymatic conjugation of GSH and reactive electrophiles. Since GSH conjugation represents the major pathway of elimination of BP epoxides in the lung, our results offer a possible explanation for the cocarcinogenicity of SO2 with PAHs. These data suggest that the sulfitolysis reaction of sulfite is the common reaction mechanism mediating the underlying biochemical reactions leading to both the toxic and cocarcinogenic properties of SO2. Quantitation of sulfitolysis products and their interaction with cellular processes should provide a coherent scheme relating SO2 and sulfite toxicity among animal species and humans.
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PMID:Covalent reactions in the toxicity of SO2 and sulfite. 376 76

The pulmonary influx of cytotoxic inflammatory cells, normally, in response to external toxins, is now thought to be etiologic in many of the disease syndromes of man, such as bronchitis and emphysema. Many types of effector inflammatory cells are involved, e.g., eosinophils, neutrophils, T-lymphocytes, monocytes. The diseases are characterized either by tissue destruction or by tissue hyperplasia. Agents which initiate the influx and cytotoxic secretions by these cells are legion and in general are not cell-specific. They include agents, such as phorbol esters, formyl peptides-complement fragments, elastin fragments, fatty acids (leukotrienes) as well as many uncharacterized excretions of inflammatory cells themselves, which react with specific receptors on the inflammatory cells, and secreted proteins such as fibronectin. Other agents, such as linoleic acid, digitonin and hydroxy fatty acids which are not bound by specific receptors also activate motility of inflammatory cells. The precise role of the above multiple cytotoxins in specific cellular fluxes in most pulmonary disease remains undefined. Similarly, the mechanism of cytotoxicity used by specific invading cells in specific pulmonary syndromes remains unclear. In general, macrophages are thought to destroy using specific proteases, neutrophils use oxidant radicals and proteases and eosinophils use basic surface active peptides. T-cells kill by unknown mechanisms. However, in specific clinical syndromes, it is usually not clear which cell is the cytotoxic culprit, nor is the mechanism of destruction usually known.
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PMID:Control of cellular influx in lung and its role in pulmonary toxicology. 637 3

In order to demonstrate how patients with immotile cilia syndrome (ICS) are associated with lower respiratory tract inflammation, bronchoscopy and fractionated BAL were performed on eight ICS patients. Their VC was 84.5 +/- 16.7% (mean +/- SD) and FEV1 73.1 +/- 19.9% of predicted. Endobronchial signs of bronchitis were observed in all patients. The total cell concentrations in the BAL fluid were increased, compared to healthy nonsmokers (n = 10), both in the bronchial (BP) and alveolar portion (AP) (p < 0.01 for both). In the BP, this was mainly due to a high concentration of neutrophils (p < 0.001), whereas in the AP, the concentrations of lymphocytes (p < 0.01) as well as all types of granulocytes (p < 0.001-0.01) were elevated. The signs of active inflammation in the lower respiratory tract were confirmed by the concomitantly elevated (p < 0.001-0.05) concentrations of the soluble BAL components albumin, fibronectin and hyaluronan. Thus, the inflammatory response is not restricted to the ciliated conducting airways, but also occurs in the alveolar space and results-surprisingly-in only a slightly impaired lung function.
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PMID:The immotile cilia syndrome: characterization of the inflammatory response in nonsmoking patients with dysfunction of the cilia. 893 49

One hundred and forty five patients with different forms of dust-induced lung disease and 57 controls having no contacts with industrial aerosols were examined. It was ascertained that clinical and functional evidence cannot predict the course of the disease and the development of infectious complications (silicotuberculosis, mechanic bronchitis). Impaired humoral immunity and nonspecific resistance in dust-induced lung disease depend on the type of disease and predispose to infectious complications. Predisposition to occupational lung diseases (pneumoconioses, mechanical bronchitis) is associated with increases in the concentrations of plasma fibronectin and serum IgA and a decrease in serum mucin antigen levels. In chronic mechanical bronchitis, there were lower activities of lysozyme and complement and elevated serum IgM and IgG concentrations. Fibronectin, total IgE and the inflammatory marker the mucin antigen 3EG5 are involved in immunological inflammation in dust-induced lung disease. It is worth of determining the factors of humoral immunity and nonspecific resistance in workers contacting with high concentrations of industrial aerosols and in patients with dust-induced diseases to make a precise assessment of the time course of changes in a pathological process and to define a risk for infectious complications.
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PMID:[Immunological changes in dust-induced lung diseases]. 1131 68


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