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)

A technique used for study of permeability and vasodilation in the middle ear has been adapted to study the response of nasal mucosa to common inflammatory mediators involved in the natural production of allergic or infectious rhinitis. All of the mediators tested (histamine, prostaglandin E1, bradykinin, the C3a fraction of complement, Escherichia coli endotoxin, and lysozyme) were found to increase nasal permeability to the isotopic tracer 99mTc as the pertechnetate ion. Histamine increased the permeability of nasal mucosa to technetium-labeled plasma protein. Results indicate that the nasal mucosa is approximately ten times as permeable to the pertechnetate ion as middle ear mucosa. Nasal mucosa was also noted to be permeable to protein, even in the absence of inflammatory mediator, in contrast to prior studies of middle ear mucosa that showed little or no permeability in the absence of inflammatory mediator. In almost all cases, a corresponding change in vasodilation accompanied permeability changes.
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PMID:Effect of inflammatory mediators on nasal mucosa. 32 89

147 samples of punctured middle ear effusion fluid from cases of otitis media with effusion and 150 samples from patients with acute purulent otitis media were tested for lysozyme activity. In otitis media with effusion the concentration was 182.0 U/ml, in acute otitis 433.8 U/ml. The lysozyme concentration in otitis media with effusion depended upon the nature of the effusion. Serous fluid showed an activity of 124.8 U/ml and mucoid 311.6 U/ml, respectively. In culture-positive cases of acute otitis media the lysozyme level was 423.4 U/ml. Culture-negative cases showed about the same concentration, 438.3 U/ml. The possible role of lysozyme in defence systems of the middle ear is discussed.
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PMID:Lysozyme activity and immunoglobulins in middle ear effusion fluid in acute purulent otitis media and in otitis media with effusion. 41 70

Biochemical composition of middle ear effusions (MEE) and serum was compared both in experimentally induced middle ear inflammation in squirrel monkeys and in otitis media in humans. The MEE and serum protein concentrations were similar in the animal experiments. In human MEE the total protein concentration of both serous and mucoid effusions was higher than the proteins of the serum. High concentrations of potassium and lower concentrations of glucose in human MEE than in serum were also observed. Activities of various oxidative (lactate dehydrogenase, malate dehydrogenase) and hydrolytic (leucine aminopeptidase, alkaline and acid phosphatase, and lysozyme) enzymes in MEE and serum were compared. The ratio of enzyme activity between MEE and serum (MEE/Serum) was greater than one in all enzymes studied. Mucoid MEE had higher activity of enzymes than serous effusions in general. Lactate dehydrogenase isoenzyme patterns were compared on electropherogram. Isoenzyme fractions 1 and 2 were each smaller in MEE than in serum whereas 4 and 5 had a significantly higher activity in MEE than in serum. Higher activities of enzymes in MEE as compared with serum are consistent with the hypothesis that MEE results from inflammatory processes occurring in the middle ear cavity. The enzymes of MEE seem to have multiple origins, namely, 1) enzymes normally present in blood, 2) enzymes from the inflamed middle ear mucosa, and 3) enzymes from leucocytes present in effusions.
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PMID:Biochemical characteristics of middle ear effusions. 81 35

Lysozyme was demonstrated by an immunocytochemical technique in the biopsied mucosa obtained from the promontory of the fifteen patients who had chronic middle ear effusions. Lysozyme was localized in the mucigen granules of the secretory cells, as well as in the specific granules of the polymorphonuclear neutrophilic leukobytes (PMN) and macrophages. The specimens obtained from patients with mucous effusion showed numerous secretory cells that contained lysozyme, in sharp contrast to the serous type in which only a few secretory cells could be found. The present morphological finding was in agreement with the biochemical finding which demonstrated higher lysozyme level in mucous effusions than that of the serous type. It was concluded that human middle ear mucosa provided lysozyme and that its secretion was active in serous otitis media, particularly of mucoid type.
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PMID:Secretory lysozyme of the human middle ear mucosa: immunocytochemical localization. 94 8

Activities of various oxidative (LDH, MDH) and hydrolytic (LAP, alkaline- and acid phosphatase, and lysozyme) enzymes in serous middle ear effusions (MEE) and serum from patients with serous otitis media were studied. The ratio of enzyme activity between MEE and serum (MEE/serum) was greater than one for all enzymes studied indicating a higher activity of these enzymes in MEE than in serum. These findings are consistent with a hypothesis suggesting the release of enzymes from inflammatory processes in the middle ear cavity. These enzymes presumably originate from 1) enzymes normally present in blood, 2) release of enzymes from inflamed middle ear mucosa, 3) release of enzymes from inflammatory cells present in the effusions.
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PMID:Certain oxidative and hydrolytic enzymes in the middle ear effusion in serous otitis media. 98 18

Analyses of effusions and sera from patients with otitis media with effusion demonstrated local production in the middle ear of lysozyme, IgA and IgG. The effusion IgM was markedly elevated in some patients, also indicating local production. Complement C3 with rare exception was significantly lower in effusions than sera, suggesting utilization of complement in the middle ear, perhaps in conjunction with antibodies. The presence of high levels of lysozyme and immunoglobulins in effusions correlates with the low isolation rate of microorganisms in culture and may influence survival of organisms in the middle ear.
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PMID:Antimicrobial factors and bacterial correlation in chronic otitis media with effusion. 126 37

A review of available histological, histochemical and ultrastructural data on middle ear mucosa and the Eustachian tube was made to provide a broad cellular basis for understanding middle ear effusions. The presence of mucociliary defense system in a large part of the Eustachian tube and middle ear is seen as the first line of defense. Secretion by the mucosa has a profound biological significance. Immunoglobulins A, G, and even E and M are produced locally by the mucosa and may contribute to the immunodefense of the middle ear. Secretory lysozyme is also produced by the mucosa and may contribute enzymatic defense of the ear. Mucosal immunoglobulins and lysozyme are significantly elevated in the effusions, which would imply that local defense systems are hyperactive in OME. It also appears that these increases are related to the increase of the secretory cell population. It is also suspected that auditory surface-active agent is produced locally and may facilitate normal function of the tube. The middle ear also can transport macromolecules very rapidly across intact mucosal epithelium. The large numbers of tissue and wandering macrophages found in the mucosa and effusions would also imply that the middle ear is capable of efficient phagocytosis, which may be involved in processing antigen.
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PMID:Functional morphology of the mucosa of the middle ear and Eustachian tube. 126 66

Most Streptococcus pneumoniae strains are killed by very low concentrations of penicillin and other beta-lactam antibiotics, yet middle ear inflammation and effusion persist for days to weeks after treatment in most cases of pneumococcal otitis media. To study the effect of beta-lactam antibiotic treatment on pneumococci and the middle ear inflammatory response during pneumococcal otitis media, we measured concentrations of pneumococci, inflammatory cells, and lysozyme in middle ear fluid (MEF) by using the chinchilla model. Procaine penicillin G given intramuscularly 12 and 36 h after inoculation of pneumococci into the middle ear caused a significant acceleration in the MEF inflammatory cell concentration compared with that in untreated controls, with a significant peak in the inflammatory cell concentration 24 h after pneumococcal inoculation. The lysozyme concentration in MEF also increased more rapidly in treated than in control animals. Viable pneumococci were not detected in MEF after the second dose of penicillin, but the total pneumococcal cell concentration remained unchanged for at least 45 days. Therefore, penicillin treatment accelerated middle ear inflammation while killing pneumococci, but treatment did not accelerate clearance of the nonviable pneumococcal cells from MEF. Further studies will need to define the contribution of these responses to acute and chronic tissue injury.
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PMID:Penicillin treatment accelerates middle ear inflammation in experimental pneumococcal otitis media. 156 82

The pathogenesis of middle ear inflammation caused by Streptococcus pneumoniae was explored in the chinchilla model with different pneumococcal cell wall (CW) preparations, including isolated native CW, M1 muramidase CW (M1-CW) digest, amidase CW digest, and M1 peptidoglycan (M1-PG) digest. Inflammatory cell and lysozyme concentrations in middle ear fluid (MEF) were measured between 6 and 72 h after the middle ears were inoculated with one of the preparations or sterile saline. Middle ear histopathology was measured quantitatively at 72 h. Native CW, M1-CW digest, and amidase-CW digest caused significantly more inflammatory cell influx and lysozyme accumulation in MEF than saline did. M1-PG digest also caused more inflammatory cell influx and lysozyme accumulation in MEF than saline did but caused less inflammation than native CW or either CW digest. Epithelial metaplasia was significantly greater in ears inoculated with native CW than in ears inoculated with the CW or PG digest or with saline. Pneumococcal CW is, therefore, the principal factor that initiates middle ear inflammation in acute pneumococcal otitis media, and CW teichoication seems to be important in initiating this response.
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PMID:Role of the bacterial cell wall in middle ear inflammation caused by Streptococcus pneumoniae. 161 50

Streptococcus pneumoniae is an important bacterial pathogen in the pathophysiology of otitis media. To elucidate the inflammatory responses that occur during pneumococcal otitis media, the kinetics of the biochemical and cytologic middle ear responses to heat-killed encapsulated and nonencapsulated pneumococci were studied in the chinchilla model. Inoculation of the middle ear cavity with at least 10(6) S pneumoniae cells induced an early, brief vascular response with leakage of small (albumin) followed by larger (alpha 2-macroglobulin) proteins, followed by sustained influx of acute inflammatory cells and lysozyme. The threshold for a sustained lysozyme response was 1,000 times lower for nonencapsulated than for encapsulated pneumococci. These results indicate that nonviable S pneumoniae organisms with an intact envelope initiate the middle ear inflammatory response. Therefore, interventions that enhance the clearance of pneumococcal cells from the middle ear may reduce the inflammatory response and prevent chronic middle ear inflammation.
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PMID:Pathophysiology of Streptococcus pneumoniae otitis media: kinetics of the middle ear biochemical and cytologic host responses. 170 82


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