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)

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

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

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

Middle ear infection with Streptococcus pneumoniae is important in the pathogenesis of acute and chronic otitis media, and lysozyme in middle ear fluid (MEF) is an important inflammatory mediator in this disease. To determine the source of lysozyme during the early period of acute pneumococcal otitis media, chinchillas were irradiated to induce neutropenia, and their middle ears were inoculated with heat-killed, encapsulated pneumococci. The number of inflammatory cells and concentration of lysozyme were measured in MEF between 6 and 72 hours after inoculation. In pneumococcus-inoculated ears, the mean number of inflammatory cells but not lysozyme was significantly lower in MEF from irradiated animals than that from nonirradiated animals at 6 hours. Since lysozyme accumulated in MEF before the influx of inflammatory cells in irradiated animals, the initial release of this inflammatory mediator is most likely not from inflammatory cells; and mucosal epithelial cells, the only other known source of lysozyme in the middle ear environment, were the probable source induced by the direct stimulation of pneumococci. Inflammatory cells may contribute lysozyme later in the inflammatory response, since cellular and lysozyme concentrations in irradiated and nonirradiated animals were similar between 24 and 72 hours. These results suggest that future therapeutic interventions to limit middle ear inflammation in acute otitis media may need to recognize the direct action of pneumococcal cells or their envelope components on middle ear epithelium.
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PMID:Middle ear fluid lysozyme source in experimental pneumococcal otitis media. 206 74

Endotoxin levels and lysosomal protease (collagenase, cathepsin B, and lysozyme) activity were measured in 104 middle ear effusions (MEEs) from patients with otitis media with effusion (OME). The MEE samples were classified into four groups: pediatric serous, mucoid, and acute, and adult serous. Endotoxin levels and lysosomal protease activity in MEEs were significantly different in the following order: adult less than serous less than mucoid less than acute groups, indicating that both endotoxin and lysosomal proteases are more closely related to the pathogenesis of pediatric chronic OME than to adult OME. In pediatric serous and mucoid effusions, endotoxin level had a significant correlation with activity of the lysosomal proteases. In conclusion, endotoxin enhances leukocyte infiltration into the middle ear, and lysosomal proteases released from leukocytes damage the middle ear mucosa and thereby prolong mucosal inflammation, which may be responsible for delayed recovery from acute OME.
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PMID:Endotoxin and lysosomal protease activity in acute and chronic otitis media with effusion. 215 54

Lysozyme concentrations in middle ear effusion and serum were determined in patients with otitis media with effusion. Lysozyme concentrations in middle ear effusion were significantly higher than in serum. Children with mucoid otitis media showed significantly higher levels of lysozyme in middle ear effusion than children with serous otitis media and adults with otitis media with effusion. Higher levels of lysozyme were observed in the group of children younger than 5 years old compared with the age group of 6- to 10-year-olds. Lysozyme concentrations of middle ear effusion in adults were significantly lower than those of mucoid otitis media in children. These results indicate that lysozyme plays an important role in the disease process of otitis media.
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PMID:Lysozyme levels in middle ear effusion and serum in otitis media. 229 41

We studied the contribution of pneumococcal cell wall to the pathogenesis of otitis media in chinchillas after middle ear inoculation of killed, encapsulated type 7F Streptococcus pneumoniae; killed, unencapsulated R6 S. pneumoniae; and isolated R6 pneumococcal cell wall. Ears inoculated with encapsulated and unencapsulated pneumococci had significantly higher concentrations of polymorphonuclear and mononuclear leukocytes and lysozyme in middle ear fluid and developed more epithelial metaplasia and granulation tissue than did saline-inoculated ears. The mean concentration of lysozyme in middle ear fluid was higher in ears inoculated with killed, unencapsulated than encapsulated pneumococci. The middle ear mucoperiosteum of ears inoculated with pneumococcal cell wall showed significantly more polymorphonuclear leukocytes, epithelial metaplasia, subepithelial congestion, and granulation tissue than did control ears. Because nonviable, unencapsulated pneumococci and pneumococcal cell wall caused middle ear inflammation in the chinchilla model of otitis media, it is possible that cell envelope and cell wall components released during bacterial lysis may contribute to chronic otitis media with effusion in humans.
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PMID:The contribution of pneumococcal cell wall to the pathogenesis of experimental otitis media. 333 9


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