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)

Major outer membrane antigens, proteins, and lipopolysaccharides (LPSs), from nontypable Haemophilus influenzae were characterized and examined as targets for complement-dependent human bactericidal antibodies. Outer membranes from two nontypable H. influenzae isolates that caused otitis media and pneumonia (middle ear and transtracheal aspirates) were prepared by shearing organisms in EDTA. These membranes were compared with membranes prepared independently by spheroplasting and lysozyme treatment of whole cells and found to have: similar sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) patterns of the proteins; identical densities (rho = 1.22 g/cm3); and minimal d-lactose dehydrogenase activity indicating purity from cytoplasmic membranes. Outer membranes were solubilized in an LPS-disaggregating buffer and proteins were separated from LPS by molecular sieve chromatography. The SDS-PAGE patterns of outer membrane proteins (OMPs) from the two strains differed in the major band although other prominent bands appeared similar in molecular weight. LPS prepared by hot phenol water extraction of each of the strains contained 45% (pneumonia isolate) and 60% (otitis isolate) lipid (wt/wt), 49% and 50% carbohydrate (wt/wt), respectively, and less than 1%, 3-deoxy-manno octulosonic acid. Immunoglobulin M (IgM) purified from normal human serum (NHS) plus complement was bactericidal for both strains. Purified immunoglobulin G (IgG) from NHS killed the middle ear isolate and immune convalescent IgM from the serum of the patient with pneumonia killed his isolate. NHS or convalescent serum were absorbed with OMPs and LPS (0.6-110 micrograms) from each of the strains and immune specific inhibition of bactericidal antibody activity by each antigen was determined. OMPs from the pulmonary isolate inhibited bactericidal antibody activity directed against the isolate in both NHS (1.5 microgram of antigen) and immune serum (0.75 microgram of antigen). OMPs (60 micrograms) from the ear isolate also inhibited bactericidal activity in the respective immune serum. LPSs exhibited minimal inhibition (greater than 110 micrograms). Three human sera (two normal, one immune) were selectively depleted of 80% of antibody activity against OMPs (measured by enzyme-linked immunosorbent assay) by affinity chromatography using OMPs from the pulmonary isolate coupled to a solid phase. These OMP antibody-depleted sera also showed an 88% reduction of bactericidal activity against this strain. Immunopurified antibody against OMPs eluted from the solid phase was bactericidal.
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PMID:Characterization of antigens from nontypable Haemophilus influenzae recognized by human bactericidal antibodies. Role of Haemophilus outer membrane proteins. 387 75

Mononuclear phagocytes are cells common in the subepithelial space of the mucosa of the middle ear and in middle ear effusion during an attack of otitis media. Here we review studies to date on biological potentials of aural macrophages in the pathogenesis of otitis media. The origin of aural macrophages may be in the circulating pool of monocytes in the blood, in the pre-existing population of macrophages in the mucosa of the middle ear, in proliferation of macrophages in the middle ear, or in nasopharyngeal and tonsillar tissues. Macrophages demonstrate great phagocytic activity in eliminating tissue-debris, bacteria, and viruses. It seems likely that the secretory products of macrophages--such as lysozyme, components of complement, prostaglandins, collagenase, and other biologically active agents--play an important part in the pathogenesis of otitis media. There is also evidence available that aural macrophages play an important role in the regulation of lymphocytic response to antigens in active otitis media.
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PMID:Aspects of biological potentials of mononuclear cells in middle ear effusions. 639 5

The sequential cytologic and biochemical events of middle ear effusion (MEE) were studied in experimental models of serous otitis media (SOM) and purulent otitis media (POM) in chinchilla. In the SOM model, the initial appearance of neutrophils was followed by macrophages. In the POM model, neutrophils were the predominant cells in MEE and the number of neutrophils was about 100-fold higher than in the SOM model. The activity of lysozyme in MEE was higher in POM than in SOM and correlated with the number of neutrophils and mononuclear phagocytes. The results of the present study suggest that neutrophils and mononuclear phagocytes are one of the main sources for lysozyme levels in MEE during otitis media.
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PMID:Biochemical pathology of otitis media with effusion. 659 70

Experimental otitis media was produced in chinchillas by eustachian tube obstruction or pneumococcal infection. Sequential changes in the histology of the middle ear mucosa and enzyme profile of the middle ear effusions (MEE) were studied. In serous otitis media (SOM) which followed tubal obstruction, the subepithelial space was widened by edema and capillary dilatation, and the middle ear space was filled with serous fluid. Slight hyperplasia of epithelial cells was also observed. The subepithelial space remained widened with mild fibrous change and capillary dilatation, and slight hyperplasia of epithelial cells persisted 42 days after obstruction. In purulent otitis media (POM), which followed inoculation of pneumococci into the middle ears, metaplasia of the epithelial layer from flat to columnar cells was observed. The subepithelial space was widened with loose fibrous connective tissue proliferation, vascular dilatation and inflammatory cell infiltration. Both lactate dehydrogenase (LDH) and lysozyme levels in MEE were higher in the POM group than in the SOM group. When bacterial enzymes, hyaluronidase and lipase activity were measured in MEE and plotted together with the percentage of positive culture of the MEE at different times after the experimental infection, the enzyme activities decreased with the clearing of bacteria and along with the resorption of inflammatory changes of middle ear mucosa evidenced by histology. In human MEE studies, immunoglobulins (IgG, IgA, IgM) of MEE were higher than in serum except IgM in serous MEE. The IgG content of MEE in the culture-negative group was higher than in the culture-positive group. Possible mechanisms for this difference were discussed.
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PMID:Biochemical and immunochemical characteristics of middle ear effusions in relation to bacteriological findings. 677

The transfer of host defence capacity to the human offspring provides a remarkable model of passive transfer of immunity. In fact it may also provide an example of active immunization. The transfer of mucosal protection via breast feeding offers many additional advantages for the mother and infant. Through its contraceptive effects it increases the spacing between births, thus diminshing the infant mortality and the burden on the mother. It also enhances bonding between mother and child, it seems to increase the IQ and school result of the infant and might decrease the risk of certain malignancies and perhaps of juvenile diabetes. A fully breast-fed infant receives as much as 0.5-1 g of secretory immunoglobulin A (SIgA) antibodies daily, the predominant antibody of human milk. This can be compared to the production of some 2.5 g of SIgA per day for a 60 kg adult. These SIgA antibodies have been shown to protect against Vibrio cholerae, ETEC, Campylobacter, Shigella and Giardia. Furthermore, milk is rich in receptor analogues for certain epithelial structures which microbes need for attachment to host tissues as an initial step in infections. Thus the adherence of Haemophilus influenzae and pneumococci for example to retropharyngeal cells is efficiently inhibited by human milk. This may be one explanation for the fact that breast-fed babies have less otitis media than the non-breast-fed. Other milk factors like lysozyme and lactoferin may contribute to the host defence, but this has not yet been well defined. However, human milk also supports the well-being of the infant by being anti-inflammatory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Breast feeding: overview and breast milk immunology. 782 63

Infection and inflammation of the middle ear cleft are important factors in the pathogenesis of secretory otitis media. Although high percentages of negative cultures are confronted in many studies, strong evidence pointing to the infectious nature of this disease could not be overlooked. Many authors agree about the failure of conventional culture methods in identifying the responsible pathogen or pathogens. Besides, some agents, such as some kinds of antibiotics, lysozyme, and perhaps some undetected materials, are capable of changing bacterial behavior and consequently the clinical course. Effusions taken from 40 ears with secretory otitis media were cultured by means of conventional brain-heart infusion broth and special hypertonic thioglycollate broth. Strikingly, bacterial L-forms were detected in 6 specimens in thioglycollate broth, with no growth in the conventional broth. We concluded that these atypical forms of bacteria, the L-forms, may play an important role in the bacteriologic aspect of secretory otitis media.
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PMID:Preliminary report on L-forms: possible role in the infectious origin of secretory otitis media. 820 9

The exact causative factor(s) of bone erosion in cholesteatoma are not known. In recent years, the possible role of cytokines has drawn attention. Since the studies on cytokines in cholesteatoma are limited and depend on histopathological methods, the present work approached this subject by biochemical determination of TNF-alpha lysosomal enzymes, acid phosphatase (total and tartrate resistant), cathepsin B, leucyl aminopeptidase lysozyme together with non-lysosomal enzymes calpain I and II in 50 cholesteatoma samples (epithelial and subepithelial tissues) in comparison with 14 normal skin samples from the external ear canal. The study revealed significantly increased levels of all previous indices in cholesteatoma epithelium and subepithelial tissues compared with healthy skin. The levels of these indices reflected the clinical severity of the disease as reflected by their significant increase in cases with erosion of two or three ossicles, erosion of dural plate, sinus plate and facial canal and more extensive cholesteatoma. It is likely that TNF-alpha acts both directly by causing bone erosion and indirectly by stimulating the release of lysosomal enzymes. The latter mechanism is supported by the significant correlations observed between TNF-alpha and lysosomal enzymes. The non-lysosomal enzymes calpain I and II seem to participate in the bone erosion associated with cholesteatoma by their involvement in collagen destruction. Due to the suggested role of TNF-alpha in bone destruction associated with cholesteatoma the use of anti-inflammatory drugs should be taken into consideration in otitis media to diminish bone destruction. Similarly, antibiotics should be used to prevent the deleterious effects of bacterial endotoxin.
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PMID:Clinical and biochemical studies of bone destruction in cholesteatoma. 876 71

Moraxella catarrhalis is a normal resident of the human nasopharyngeal flora, but it is also isolated from middle ear fluid of acute otitis media and otitis media with effusion patients. To determine whether M. catarrhalis has direct pathogenicity in the middle ear, heat-killed M. catarrhalis was inoculated into the middle ear bullae of guinea pigs, and the inflammatory response was investigated. Middle ear mucosal histopathology observed in M. catarrhalis-inoculated ears included subepithelial edema, capillary dilatation, thickening of lamina propria mucosa, inflammatory cell and erythrocyte infiltration into the lamina propria mucosa. Inflammatory cell numbers, lysozyme and myeloperoxidase concentrations in the middle ear washing suspensions of M. catarrhalis-inoculated ears were significantly higher than control ears throughout the experiment. Therefore, nonviable M. catarrhalis induced middle ear inflammation and mucoperiosteal histopathology, which might be caused by direct injury of the nonviable bacteria (e.g. lipooligosaccharide or outer membrane proteins) and metabolic products of inflammatory cells.
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PMID:Experimental otitis media induced by nonviable Moraxella catarrhalis in the guinea pig model. 925 51

Streptococcus pneumoniae is the most frequent microbe causing middle ear infection. The pathophysiology of pneumococcal otitis media has been characterized by measurement of local inflammatory mediators such as inflammatory cells, lysozyme, oxidative metabolic products, and inflammatory cytokines. The role of cytokines in bacterial infection has been elucidated with animal models, and interleukin (IL)-1beta, IL-6, and IL-8 and tumor necrosis factor alpha (TNF-alpha) are recognized as being important local mediators in acute inflammation. We characterized middle ear inflammatory responses in the chinchilla otitis media model after injecting a very small number of viable pneumococci into the middle ear, similar to the natural course of infection. Middle ear fluid (MEF) concentrations of IL-1beta, IL-6, IL-8, and TNF-alpha were measured by using anti-human cytokine enzyme-linked immunosorbent assay reagents. IL-1beta showed the earliest peak, at 6 h after inoculation, whereas IL-6, IL-8, and TNF-alpha concentrations were increasing 72 h after pneumococcal inoculation. IL-6, IL-8, and TNF-alpha but not IL-1beta concentrations correlated significantly with total inflammatory cell numbers in MEF, and all four cytokines correlated significantly with MEF neutrophil concentration. Several intercytokine correlations were significant. Cytokines, therefore, participate in the early middle ear inflammatory response to S. pneumoniae.
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PMID:Middle ear fluid cytokine and inflammatory cell kinetics in the chinchilla otitis media model. 1008 40

The sterility of the eustachian tube and tympanic cavity of normal individuals is maintained not only by the adaptive immune system, but also by the mucociliary system and the antimicrobial molecules of innate immunity. Mucin production and periciliary fluid homeostasis are essential for normal mucociliary function and dysfunction of this system is an important risk factor for otitis media. The secreted antimicrobial molecules of the tubotympanum include lysozyme, lactoferrin, beta defensins, and the surfactant proteins A and D (SP-A, SP-D). Defects in the expression or regulation of these molecules may also be the major risk factor for otitis media.
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PMID:Cell biology of tubotympanum in relation to pathogenesis of otitis media - a review. 1116 58


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