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)

Neuropeptides such as substance P are implicated in inflammation mediated by sensory nerves (neurogenic inflammation), but the roles in disease of these peptides and the peptidases that degrade them are not understood. It is well established that inflammation is a prominent feature of several airway diseases, including viral infections, asthma, bronchitis, and cystic fibrosis. These diseases are characterized by cough, airway edema, and abnormal secretory and bronchoconstrictor responses, all of which can be elicited by substance P. The effects of substance P and other peptides that may be involved in inflammation are decreased by endogenous neutral endopeptidase (NEP; also called enkephalinase, EC 3.4.24.11), which is a peptidase that degrades substance P and other peptides. In the present study, we report that rats with histories of infections caused by common respiratory tract pathogens (parainfluenza virus type 1, rat corona-virus, and Mycoplasma pulmonis) not only have greater susceptibility to neurogenic inflammatory responses than do pathogen-free rats but also have a lower activity of NEP in the trachea. This reduction in NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentrations of substance P to reach tachykinin receptors in the trachea. Thus decreased NEP activity may exacerbate some of the pathological responses in animals with respiratory tract infections.
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PMID:Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections. 254 62

Airway smooth muscle contraction and the extreme sensitivity of the airway smooth muscle responses to various stimuli are accepted as key factors in the pathogenesis of asthma and are recognized to be important in other diseases (e.g., bronchitis and cystic fibrosis). A Workshop on Airway Smooth Muscle sponsored by the National Heart, Lung and Blood Institute (September 25 to 27, 1983) identified various avenues of future research. Smooth muscle anatomists pointed to the paucity of quantitative information on airway smooth muscle structure, especially electron microscopic information and details of the neural arrangement. Investigations of the neural network, similar to those that have led to important discoveries in the gut, are urgently needed. Now that intramural ganglia can be studied electrophysiologically (and in vivo!), new information concerning possible local neural modulation can be examined. A similar lack of information was found in the biochemical study of airway smooth muscle. Among potential causes of abnormalities in asthmatic muscles are alterations in membrane channels and pumps, receptor transduction processes, cGMP-mediated processes, and other metabolic pathways. Inflammation and inflammatory mediators appear to play important roles in disease of airway smooth muscle. Utilization of cell isolation and culture, and immunologic and other cell biologic and biochemical methods will accelerate the study of the various cells in the airways, their interactions, and their roles in disease. Of special potential importance are peptide and lipid mediators produced by various airway cells. Development of synthetic analogues and antagonists, including monoclonal antibodies, will provide more specific tools for dissecting these cell-to-cell interactions. Regardless of the level of study--from examination of the whole organism to molecular mechanisms--the fact is that there is no entirely satisfactory animal "model" of asthma or asthmatic muscle, presumably because we do not fully understand the etiology and pathogenesis of asthma. This makes it all the more important to take appropriate opportunities to obtain tissue from asthmatics for laboratory study. Relatively simple, careful studies of asthmatic smooth muscle may prove important, unique insights into its possible abnormalities.
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PMID:Workshop on airway smooth muscle. Summary of a conference held September 25-27 1983. 257 64

Patients with cystic fibrosis suffer from a chronic, progressively destructive bronchitis characterized by colonization of the airways by Pseudomonas aeruginosa. Cell wall lipopolysaccharides from P. aeruginosa may stimulate secretion of cytokines such as tumor necrosis factor alpha (TNF alpha) by monocytes/macrophages. We found elevated levels of TNF alpha (150 +/- 60 pg/ml), interleukin-1 alpha (144 +/- 205 pg/ml), and interleukin-1 beta (62 +/- 100 pg/ml) in plasma from 25 patients with cystic fibrosis. In patients with less advanced disease, elevated plasma levels of TNF alpha correlated with high levels of complexes between neutrophil elastase and alpha 1-proteinase inhibitor, suggesting that TNF alpha may be a mediator of neutrophil degranulation. TNF alpha, by its chemotactic effect on neutrophils, may also contribute to the massive influx of neutrophils into and around the bronchial tree. Our findings raise the questions whether in patients with cystic fibrosis TNF alpha acts as cachectin and whether it mediates the anorexia that often results in weight loss.
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PMID:Relation between tumor necrosis factor-alpha and granulocyte elastase-alpha 1-proteinase inhibitor complexes in the plasma of patients with cystic fibrosis. 222 2

The physical and chemical properties of bronchial epithelial mucus depend on its special mix of macromolecules and lipid constituents: these are different in the normal airway under baseline conditions from one stimulated acutely, and show major modification in disease. Since the last conference, density gradient ultracentrifugation has been extended to the study of normal bronchial mucus in addition to that of sputum from patients with chronic bronchitis, cystic fibrosis and asthma, and has revealed striking differences between the chemical profiles of normal and hypersecretory mucus. Normal mucus represented individual bronchial aspirates, obtained at fiberoptic bronchoscopy from healthy human volunteers (non-smokers), aspirates from normal dogs (before SO2 exposure in a canine model of SO2 induced bronchitis) and secretions released in vitro by human bronchial and canine tracheal explants. Mucus 'in transition' included aspirates from otherwise healthy smokers and from dogs early in irritation. Hypersecretory mucus included, besides those mentioned above, aspirates from dogs that had developed bronchitis and the excessive mucus produced by some patients with acute quadriplegia. Lipids. In normal mucus, human (unpooled) and canine, neutral lipids are the predominant species, with lesser amount of phospholipids: no glycolipids are detected. The first qualitative change on irritation, even before macromolecular yield increases, is appearance of glycolipids. In hypersecretory mucus, human (including quadriplegics) or canine, glycolipids are detected in appreciable amounts and often are the predominant species: they include complex forms such as sialic acid containing gangliosides. Organ and cell culture studies establish that these lipids are produced by airway epithelial cells. These lipids are important to gel formation. Glycoconjugates. A major recent advance is the recognition that normal mucus does not contain typical epithelial glycoprotein. Its glycoconjugate is of higher density with sugars typical of both glycoprotein (GP) and proteoglycan (PG) and with an amino acid profile more akin to PG (glycine greater than serine greater than threonine). In transition to hypersecretion, a 'mixed molecule' changes its sugar mix to produce a density typical of GP. In hypersecretion, the epithelial GP develops a typical buoyant density and amino acid profile (threonine greater than serine greater than glycine). Organ culture of bronchial explants, and more recently cell culture, establish that the PGs are major products of airway secretory cells. The normal airway is capable of producing glycoprotein on cholinergic stimulation. The range of glycoconjugates present in the secretion support the wide range of granule and cell features identified in vivo. Monoclonal antibody raised to a pure preparation of bronchial epithelial glycoprotein reacts with mucous cells in the surface epithelium and also in the submucosal gland in both human and canine airways.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Macromolecular and lipid constituents of bronchial epithelial mucus. 270 77

In symptomatic patients with cystic fibrosis, the recovery of bacteria in an inflammatory exudate from the lower respiratory tract is strong evidence of endobronchitis. It is not known when this chronic infection begins, the etiologic agents during infancy or the mechanism of evolution from Haemophilus influenzae and Staphylococcus aureus to Pseudomonas aeruginosa. Antibiotic administration to "suppress" the infection in relatively well patients is an unproven benefit. During an exacerbation of bronchitis, administration of appropriate antibiotics decreases sputum bacterial density and is accompanied by decreased amounts of indicators of inflammation in sputum: pulmonary function improves, particularly that reflecting medium to small airway status. In the future aggressive diagnostic procedures will be followed by therapeutic and prophylactic antibiotic administration conducted in a manner to minimize emergence of antibiotic-resistant bacteria. Adjunctive therapy, to minimize those aspects of the host response which inflict lung damage, will become standard.
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PMID:Endobronchial infection in cystic fibrosis. 270 22

Pseudomonas aeruginosa is the most prominent colonizer of the respiratory tract of patients with cystic fibrosis, but it is not known why this occurs. P. aeruginosa adheres to mucins from normal individuals, but mucins from cystic fibrosis patients have not been studied. To compare adhesion to mucins from cystic fibrosis with other mucins, we prepared highly glycosylated mucin glycopeptides from cystic fibrosis and chronic bronchitis patients by ion-exchange and gel-filtration chromatography and measured the adhesion of P. aeruginosa 1244 to these glycopeptides. We found (i) that the most mucinlike glycopeptides from P. aeruginosa-infected cystic fibrosis sputa showed less bacterial adhesion than did the corresponding bronchitis samples, (ii) that the most adhesive activity in cystic fibrosis samples came from a fraction that contains O and N glycopeptides and may be in part a degradation product of P. aeruginosa infection, and (iii) that highly glycosylated glycopeptides of the most acidic species (sialylated and sulfated) showed no adhesion at all. A single cystic fibrosis sample not infected by P. aeruginosa showed better binding in the adhesion-positive fractions than did the infected sputa. These studies suggest that cystic fibrosis mucins may be altered after infection is established, resulting in less binding to some fragments. However, since the clinical picture shows heavy mucus colonization, other receptors, such as cellular glycolipids which have been shed into mucus, may be contributing to this colonization.
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PMID:Differences in adhesion of Pseudomonas aeruginosa to mucin glycopeptides from sputa of patients with cystic fibrosis and chronic bronchitis. 277 73

During a period of 23 years (1962 to 1984) we found 197 children with stenoses of the main bronchi among 2,000 bronchological first examinations of children suffering from chronic or recurring bronchopulmonary diseases. In 75 children these stenoses were combined with those of the trachea, in 122 children they were restricted to the main bronchi. The left main bronchus showed an predominant incidence of 85 per cent. Only in 5 cases an extrabronchial cause could be established by anomalous vessels. In the main part of the patients we found intramural stenoses due to congenital circumscribed malazia or to complete aplasia of the bronchial cartilage. The clinical symptoms of a recurring obstructive bronchitis were predominating in nearly 80 per cent of the patients. By follow-up investigations of 65 children with an average duration of 8 years no deaths had occurred. Forty children (65 per cent) were without any complaints and could be physically loaded in a normal way, whereas 21 children showed persistent mild or moderate complaints. In two patients with cystic fibrosis and two others without this basic disorder bronchiectases had developed distal of the stenoses. Bronchological controls after an average follow-up of 3 1/2 years showed in 60 per cent of the children still unchanged stenoses and deforming changes of the bronchial wall distal of the stenoses in contrast to the more favourable clinical findings.
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PMID:[Significance of stenoses of the main bronchus within the scope of congenital abnormalities of the respiratory tract]. 323 94

Parents of children with cystic fibrosis have been reported to have a high prevalence of increased airway reactivity, but these studies were done in a select young, healthy, symptomless population. In the present study respiratory symptoms were examined in 315 unselected parents of children with cystic fibrosis and 162 parents of children with congenital heart disease (controls). The cardinal symptom of airway reactivity, wheezing, was somewhat more prevalent in cystic fibrosis parents than in controls, but for most subgroups this increased prevalence did not reach statistical significance. Among those who had never smoked, 38% of obligate heterozygotes for cystic fibrosis but only 25% of the controls reported wheezing (p less than 0.05). The cystic fibrosis parents who had never smoked but reported wheezing had lower FEV1 and FEF25-75, expressed as a percentage of the predicted value, than control parents; and an appreciable portion of the variance in pulmonary function was contributed by the interaction of heterozygosity for cystic fibrosis with wheezing. For cystic fibrosis parents, but not controls, the complaint of wheezing significantly contributed to the prediction of pulmonary function (FEV1 and FEF25-75). In addition, parents of children with cystic fibrosis reported having lung disease before the age of 16 more than twice as frequently as control parents. Other respiratory complaints, including dyspnoea, cough, bronchitis, and hay fever, were as common in controls as in cystic fibrosis heterozygotes. These data are consistent with the hypothesis that heterozygosity for cystic fibrosis is associated with increased airway reactivity and its symptoms, and that the cystic fibrosis heterozygotes who manifest airway reactivity and its symptoms may be at risk for poor pulmonary function.
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PMID:Pulmonary abnormalities in obligate heterozygotes for cystic fibrosis. 343 35

In this study we performed in situ hybridization using biotin-labelled total genomic DNA of Haemophilus influenzae type b as a probe on: (1) smears containing bacteria cultured in vitro: all haemophilus species that can be found in the human respiratory tract appeared to be positive and a large number of other bacterial species appeared to be negative in this in situ hybridization test; (2) sputum smears from 287 patients with bronchitis: the hybridization test was positive on all but 2 of the 44 smears derived from patients whose culture yielded haemophilus and additionally on 12 smears derived from patients, whose culture was negative; and (3) sputum smears from 7 patients suffering from cystic fibrosis (CF): the hybridization test was positive in all these 7 sputum smears, while the culture only yielded haemophilus in 3 cases. The higher sensitivity of the hybridization test compared to culturing could mainly be explained by the failure to detect haemophilus in culture caused by masking due to overgrowth by other bacteria. In conclusion the in situ hybridization test, which can be performed in only 4 h, is a sensitive and specific method for the detection of haemophilus in sputum and is particularly useful in CF patients, where overgrowth by pseudomonas often interferes with diagnosis by culturing.
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PMID:In situ hybridization for the detection of Haemophilus in sputum of patients with cystic fibrosis. 350 33

Bronchial casts were found in four children during a 2-year period at the Children's Memorial Hospital. These four children represent 0.2% of the 1,943 endoscopic cases during that time. Thirty other cases of bronchial casts have been reported previously in children 9 years of age or younger, only 12 of which were not associated with cystic fibrosis. Casts may be a complication of many diseases; cystic fibrosis, asthma, bronchitis, allergic bronchopulmonary aspergillosis, and bronchocentric granulomatosis are the most common. With the exception of cystic fibrosis, these diseases may all have an allergic pulmonary reaction as the underlying cause. In all four cases reported here, the diagnosis was made at endoscopy because the clinical picture is not dissimilar from that of bronchial foreign bodies. Management includes endoscopic removal of the cast, chest physical therapy with nebulized acetylcysteine, and an evaluation to determine the underlying condition.
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PMID:Bronchial casts in children. 381 93


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