Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

20 patients with chronic obstructive pulmonary disease who were treated in the resort of Sandanski, Bulgaria, during the autumn of 1988 were investigated for changes of some clinical, functional and immunologic indices--secretory immunoglobulins, lysozyme, serum bactericidal activity. The results revealed an improvement of the clinical indices mean in 50% of the patients, of the expiratory spirometric indices in mean 47% of the patients. Other findings were a distinct tendency towards a decrease of IgG and albumin in the saliva and an increase of the secretory IgA together with a statistically significant increase of the indices characterizing the nonspecific defence mechanisms of the lung.
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PMID:[Changes in the clinico-functional and immunological indices of patients with chronic obstructive lung disease, the allergic form, following combined climatotherapy at Sandanski health resort]. 177 59

In adults, the inability to secrete ABH blood group substances in water-soluble form has been recognized as an independent risk factor for the development of chronic obstructive lung disease. We studied 50 patients (mean age 12.1 years) with cystic fibrosis and identified 33 ABH secretors and 17 non-secretors. There was no correlation between secretor status and clinical status, spirometry measurements, salivary and serum lysozyme levels or rates of respiratory tract colonization with P. aeruginosa and S. aureus.
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PMID:ABH secretor status in cystic fibrosis--a negative report. 408 89

Addition of lysozyme (1 g/l) to sputum from patients with chronic obstructive lung disease increased the viscosity of the material significantly. The effect was prevented by addition of salt (LiCl) in the high concentration (0.25 mol/l). The sole addition of salt decreased the viscosity of native sputum. These results together with our earlier [5] studies of the interaction between the positively charged lysozyme and the negatively charged mucin molecules in model systems, indicate that lysozyme acts as a cross-linking agent in mucus by an electrostatic mechanism. Lysozyme is thus, at least partly, responsible for building up a macromolecular network giving mucus its characteristic gel-like properties.
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PMID:The importance of lysozyme for the viscosity of sputum from patients with chronic obstructive lung disease. 728 May 51

The aggregation of non-serotypable Haemophilus influenzae (NTHI) by whole saliva from patients with chronic obstructive lung disease (COLD) was investigated. Significant differences were observed between salivary aggregating activity of a control and COLD population (P < 0.001). Saliva from patients less prone to acute exacerbations had a greater capacity to aggregate bacteria compared with saliva from patients with a predilection to infection. The mechanism of saliva-mediated aggregation of NTHI was investigated and shown to be related to lysozyme content. Lysozyme activity in saliva was measured by the turbidimetric technique and results showed that patients with chronic bronchitis had increased levels of salivary lysozyme, with a subpopulation within the non-infection-prone group having greater amounts. A significant difference was observed in salivary lysozyme between controls and non-infection-prone (P < 0.005) and infection-prone (P < 0.05) patients, respectively: the non-infection-prone patients having significantly (P < 0.005) more than the infection-prone patients. There was significant correlation (r = 0.742, P < 0.001) between salivary aggregation of NTHI and lysozyme activity. Chromatographically purified human lysozyme had a similar aggregation profile to that of saliva. There was no difference in serum and saliva lactoferrin concentrations between groups, but there was a significant increase (P < 0.05) in serum lysozyme concentration in the non-infection-prone group. This study suggests that the level of salivary lysozyme derived from macrophages may play an important role in determining resistance or susceptibility to acute bronchitis.
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PMID:A possible role for lysozyme in determining acute exacerbation in chronic bronchitis. 758 99

Smoking is a risk factor for developing chronic obstructive pulmonary disease (COPD), but there are no good indicators for early identification of subjects who will develop symptomatic COPD. The aim of this study was to investigate inflammatory mechanisms related to changes in lung function and emphysematous changes on high resolution computed tomography (HRCT) in 'healthy' smokers. Subjects were 60-year-old men from a population study. Bronchoscopy was performed in 30 smokers and 18 who had never smoked. Blood tests, lung function measurements and HRCT were carried out in 58 and 34 subjects, respectively. In comparison with never-smokers, smokers had higher levels of myeloperoxidase (MPO), human neutrophil lipocalin (HNL), eosinophil cationic protein (ECP) and lysozyme in blood, higher levels of MPO, interleukin-8 (IL-8) and HNL in bronchial lavage (BL), and of IL-8, HNL and interleukin-lbeta (IL-1beta) in bronchoalveolar lavage (BAL). Smokers also had lower levels of Clara cell protein 16 (CC-16) in blood. HNL in BL and BAL showed strong correlations to other inflammatory markers (MPO, IL-8, IL-1beta). The variations in MPO in BL were explained by variations in HNL (R2 =0.69), while these variations in BAL were explained by variations in HNL and IL-1beta (R2 = 0.76). DL(CO) was the lung function variable most closely related to MPO and IL-8 in BL and BAL and to IL-1beta in BAL. In a multiple regression analysis, MPO, IL-1beta, IL-8 and CC-16 in BL and MPO in BAL contributed to the explanation of variations in DL(CO) to 41% and 22%. respectively, independent of smoking habits. In smokers with emphysematous lesions on HRCT, HNL in BAL correlated to emphysema score (r(s) = 0.71). We conclude that 'healthy' smoking men with a near normal FEV1 show signs of inflammation in the lower airways that are related to a decrease in DL(CO) and to emphysematous lesions on HRCT. This inflammation seems to be the result of both monocyte/macrophage and neutrophil activation.
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PMID:Neutrophil-associated activation markers in healthy smokers relates to a fall in DL(CO) and to emphysematous changes on high resolution CT. 1139 77

The mechanisms of bronchial secretion are an important part of the innate defense system that protects the airways against pathogens and environmental toxins. Bronchial secretions are mainly produced by goblet cells and submucosal glands but also small amounts of surfactant from clara cells and some other fluids are part of the airway epithelium fluid. Together with the ciliary system the bronchial secretions are essential for the bronchial clearance ("mucociliary clearance"). Cilia beat within a periciliary layer with low viscosity ("sol-phase"). They move the overlying mucous sheet ("gel-phase") by their tips towards the nose to remove those mucous particles together with foreign material and pathogens from the airways. The gel-layer of the airway epithelium fluid is formed mainly by water, mucins (MUC) and free proteins. Mucins are highly glycosylated macromolecules, to date more than 18 different MUC-genes have been described. In addition the airway epithelium fluids contains many antibacterial proteins and peptides including lysozyme, lactoferrin, secretory IgA, complement, beta-defensines as well as many others. Acute inflammatory or toxic stimuli can promote hypersecretion of mucins mediated by a large variety of cytokines and chemokines or even directly like some toxins. Chronic inflammatory conditions like asthma or COPD are associated with hyperplasia of goblet cells and submucosal glands thus increasing the secretory capacity of the airways. The system of mucociliary clearance forms a functional unit together with the coughing mechanisms discussed elsewhere in this journal.
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PMID:[Physiology and pathophysiology of bronchial secretion]. 1831 75

Oral immunotherapy with inactivated non-typeable Haemophilus influenzae (NTHi) prevents exacerbations of chronic obstructive pulmonary disease, but the mechanism is unclear. The aim of this study was to determine the mechanism of protection. This was a placebo versus active prospective study over 3 months in 64 smokers. The active treatment was three courses of oral NTHi given at monthly intervals, followed by measurement of bacteriological and immunological parameters. The results can be summarized: (i) NTHi-specific T cells increased in the placebo treatment group over time (P<0.05); (ii) the T cell response in the oral NTHi group started earlier than that in the placebo group (P<0.05); and (iii) serum NTHi-specific immunoglobulin (Ig)G had significantly greater variation in the placebo group (P<0.0001). The increase in antibody in placebos over time correlated with exposure to live H. influenzae (P<0.05) determined from culture of gargles; (iv) reduction in saliva lysozyme over time (P<0.05) was detected only in the oral NTHi treatment group. These data are consistent with T cell priming of gut lymphoid tissue by aspiration of bronchus content into the gut, with oral immunotherapy augmenting this process leading to enhanced bronchus protection. The evidence for protection was a stable IgG antibody level through the study in the oral NTHi treatment group, contrasting with an increase in antibody correlating with exposure of the airways to H. influenzae in the placebo group. Saliva lysozyme was a useful biomarker of mucosal inflammation, falling after oral NTHi consistent with a reduction in the level of intralumenal inflammation.
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PMID:Oral non-typable Haemophilus influenzae enhances physiological mechanism of airways protection. 2040 61

The long-term goal of our study is to identify chronic obstructive pulmonary disease (COPD)-related bronchoalveolar lavage fluid (BALF) nitroproteins to clarify COPD pathological mechanisms and to discover biomarkers of COPD. The goal of the present study was to detect the presence of, and potential roles of, nitroproteins in, human ex-smoker (without COPD) BALF samples. Nitroproteins were immunoprecipitated from two separate BALF samples, and digested with trypsin; and tryptic peptides were analyzed with matrix-assisted laser desorption/ionization (MALDI)-tandem mass spectrometry (MS/MS). Each MS/MS spectrum was composed of accumulated scans (n = 50-100). The MS/MS data were searched with BioWorks 2.0 TuboSequest in the SwissProt database to generate the amino acid sequence, which was evaluated manually. Eleven nitrotyrosine sites were identified in eight proteins, including progestin and adipoQ receptor family member III, zinc finger protein 432, proteasome subunit alpha type 2, NADH-ubiquinone oxidoreductase B14, slit homolog 1 protein, lysozyme, aldose 1-epimerase, and PTS system lactose-specific EIICB component. Each nitrotyrosine site was located within a specific protein domain and motif. Those identified nitrated proteins could be involved in multiple functional metabolic systems, including transcriptional regulation, mitochondrial complex, immune system, and energy metabolism.
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PMID:Nitroproteins Identified in Human Ex-smoker Bronchoalveolar Lavage Fluid. 2239 69

Elastic fiber injury is an important process in the pathogenesis of chronic obstructive pulmonary disease (COPD), particularly with regard to the development of pulmonary emphysema. Damage to these fibers results in uneven distribution of mechanical forces in the lung, leading to dilatation and rupture of alveolar walls. While the role of various enzymes and oxidants in this process has been well-documented, we propose that a previously unsuspected agent, lysozyme, may contribute significantly to the changes in elastic fibers observed in this disease. Studies from our laboratory have previously shown that lysozyme preferentially binds to elastic fibers in human emphysematous lungs. On the basis of this finding, it is hypothesized that the attachment of lysozyme to these fibers enhances their susceptibility to injury, and further impairs the transfer of mechanical forces in the lung, leading to increased alveolar wall damage and enhanced progression of COPD. The hypothesized effects of lysozyme are predicated on its interaction with hyaluronan (HA), a long-chain polysaccharide that is found in close proximity to elastic fibers. By preventing the binding of HA to elastic fibers in COPD, lysozyme may interfere with the protective effect of this polysaccharide against enzymes and oxidants that degrade these fibers. Furthermore, the loss of the hydrating effect of HA on these fibers may impair their elastic properties, greatly increasing the probability of their fragmentation in response to mechanical forces. The proposed hypothesis may explain why the content of HA is significantly lower in the lungs of COPD patients. It may also contribute to the design of clinical trials involving the use of exogenously administered HA as a potential treatment for COPD.
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PMID:Does lysozyme play a role in the pathogenesis of COPD? 2576 6

Bacterial infections of the respiratory tract contribute to exacerbations and disease progression in chronic obstructive pulmonary disease (COPD). There is also an increased risk of invasive pneumococcal disease in COPD. The underlying mechanisms are not fully understood but include impaired mucociliary clearance and structural remodeling of the airways. In addition, antimicrobial proteins that are constitutively expressed or induced during inflammatory conditions are an important part of the airway innate host defense. In the present study, we show that osteopontin (OPN), a multifunctional glycoprotein that is highly upregulated in the airways of COPD patients co-localizes with several antimicrobial proteins expressed in the airways. In vitro, OPN bound lactoferrin, secretory leukocyte peptidase inhibitor (SLPI), midkine, human beta defensin-3 (hBD-3), and thymic stromal lymphopoietin (TSLP) but showed low or no affinity for lysozyme and LL-37. Binding of OPN impaired the antibacterial activity against the important bacterial pathogens Streptococcus pneumoniae and Pseudomonas aeruginosa. Interestingly, OPN reduced lysozyme-induced killing of S. pneumoniae, a finding that could be explained by binding of OPN to the bacterial surface, thereby shielding the bacteria. A fragment of OPN generated by elastase of P. aeruginosa retained some inhibitory effect. Some antimicrobial proteins have additional functions. However, the muramidase-activity of lysozyme and the protease inhibitory function of SLPI were not affected by OPN. Taken together, OPN can contribute to the impairment of innate host defense by interfering with the function of antimicrobial proteins, thus increasing the vulnerability to acquire infections during COPD.
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PMID:Osteopontin That Is Elevated in the Airways during COPD Impairs the Antibacterial Activity of Common Innate Antibiotics. 2673 46


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