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)

Emphysema is believed to result from destruction of elastic fibers due to an imbalance between proteases and their inhibitors in the lung. The imbalance can arise from a primary failure of secretion of the inhibitors, as occurs in hereditary alpha-1-protease inhibitor deficiency, or as the result of complex interactions of environmental agents with the lung. Environmental agents may produce their effects by stimulating degradation of elastic fibers by neutrophils and macrophages, damaging protease inhibitors by oxidative or proteolytic mechanisms or by impairing the biosynthetic repair of damage to the connective tissue. Protease excess has also been consistently observed in purulent sputum. Since experimentally administered proteases stimulate secretion of mucus and damage mucociliary clearance, protease-antiprotease imbalance might be involved in the pathogenesis of bronchitis and bronchiectasis as well as emphysema. Because the protease inhibitors of bronchial mucus are distinct from those of the acinar units, and no hereditary deficiencies are known, there is no direct proof of this hypothesis in man.
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PMID:The biochemical pathogenesis of chronic obstructive pulmonary diseases: protease-antiprotease imbalance in emphysema and diseases of the airways. 329 71

We prepared in rabbits an antiserum against low molecular weight protease inhibitor (LMI) purified from the sputum of patients with purulent bronchitis. Using this antiserum in an immunoperoxidase staining method we found that this inhibitor was located exclusively in the serous cells of the submucosal glands of human upper and lower airways. The inhibitor was localized also in serous cells of the sublingual and submandibular glands. In contrast, LMI could not be demonstrated in the serous cells of the parotid gland. In the tissues investigated a strong association between the localization of the protease inhibitor and lysozyme was observed. Our observations indicate that the inhibitor may be present together with lysozyme as a secretory product in the serous cell granules. The possible consequences of the coexistence of these two proteins in the defense mechanism of the respiratory tract is discussed.
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PMID:Localization of low molecular weight protease inhibitor in serous secretory cells of the respiratory tract. 678 37

Corticosteroids caused a reduction in the ratio of sol-phase sputum concentration to serum concentration of albumin in 12 patients with chronic obstructive bronchitis, suggesting a reduction in protein transudation. Alpha-1-antitrypsin values followed the same pattern as those of albumin in both the control and treatment periods, confirming the similar behaviour of the two proteins. The alpha 1-antichymotrypsin ratios were on average three times higher than those of albumin in the control period, confirming the presence of local mechanisms in the lung for preferentially concentrating this protein. The sputum-to-serum ratio of alpha 1-antichymotrypsin, however, rose during steroid treatment with the result that there was a selective increase in this protease inhibitor, which may be of potential benefit to such patients.
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PMID:Effect of corticosteroids on sputum sol-phase protease inhibitors in chronic obstructive pulmonary disease. 698 37

When examined for immunological status, complement, basic endogenic protease blockers parameters, patients with infiltrative destructive tuberculosis of the lungs (IDTL) and IDTL combination with exacerbation of chronic pyo-inflammatory bronchitis, exhibited disturbances in cellular and humoral immunity, complement activity, content of alpha 1 protease inhibitor and alpha 2 macroglobulin which aggravated in combined respiratory pathology. Nonspecific aerosol treatment with native protease inhibitors (contrykal or gordox) and thymalin aroused the efficacy of etiotropic treatment and promoted normalization of the above defense systems.
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PMID:[Immunological and nonspecific reactivity in patients with infiltrative pulmonary tuberculosis associated with chronic nonspecific lung diseases]. 756 59

Chronic polypoid sinusitis is often accompanied with bronchitis, asthma and various allergies. All of these disorders have immunologic defects in common. The present study was devised to measure the genetically determined parameter of alpha-1-protease inhibitor by isoelectric focusing. Genetic polymorphism of alpha-1-antitrypsin is the source for biochemically less active types of the protease inhibitor. In this investigation the alpha-1-protease inhibitor type of 86 patients from Niedersaxony and 95 patients from Schleswig-Holstein was determined. All patients required sinus surgery as treatment for chronic polypoid sinusitis. The alpha-1-protease inhibitor deficiency types PI-MS and PI-MZ were found five times more frequently in patients from Niedersachsony and three times more often in patients from Schleswig-Holstein than in a control (normal) group of 127 subjects (p < 0.01). These findings were comparable to data in other publications. Results clearly showed a connection between alpha-1-protease inhibitor deficiency types and chronic polypoid sinusitis. These findings indicate that a genetic predisposition to chronic polypoid sinusitis is somehow correlated with the gene locus for alpha-1-protease inhibitor.
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PMID:[Genetic disposition to chronic polypoid sinusitis and alpha 1-proteinase inhibitor deficiency types]. 759 65

The spike (S) protein of the coronavirus (CoV) infectious bronchitis virus (IBV) is cleaved into S1 and S2 subunits at the furin consensus motif RRFRR(537)/S in virus-infected cells. In this study, we observe that the S2 subunit of the IBV Beaudette strain is additionally cleaved at the second furin site (RRRR(690)/S) in cells expressing S constructs and in virus-infected cells. Detailed time course experiments showed that a peptide furin inhibitor, decanoyl-Arg-Val-Lys-Arg-chloromethylketone, blocked both viral entry and syncytium formation. Site-directed mutagenesis studies revealed that the S1/S2 cleavage by furin was not necessary for, but could promote, syncytium formation by and infectivity of IBV in Vero cells. In contrast, the second site is involved in the furin dependence of viral entry and syncytium formation. Mutations of the second site from furin-cleavable RRRR/S to non-furin-cleavable PRRRS and AAARS, respectively, abrogated the furin dependence of IBV entry. Instead, a yet-to-be-identified serine protease(s) was involved, as revealed by protease inhibitor studies. Furthermore, sequence analysis of CoV S proteins by multiple alignments showed conservation of an XXXR/S motif, cleavable by either furin or other trypsin-like proteases, at a position equivalent to the second IBV furin site. Taken together, these results suggest that proteolysis at a novel XXXR/S motif in the S2 subunit might be a common mechanism for the entry of CoV into cells.
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PMID:Proteolytic activation of the spike protein at a novel RRRR/S motif is implicated in furin-dependent entry, syncytium formation, and infectivity of coronavirus infectious bronchitis virus in cultured cells. 1955 14