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)

Middle ear effusions from 100 patients (ages 6 months to 10 years) with serous otitis media were examined. The IgA, IgG, and lysozyme were demonstrated at a higher level in the effusions than the corresponding sera, indicating local production. The mucoid type contained higher level of immunoglobulins and lysozyme compared to serous type effusions. Bacteria were found in 77 percent of the effusions by means of a smear, and 52 percent yielded positive bacterial culture. The incidence of positive culture in effusions of the patients less than 6 years of age was 60 percent, while the group older than 6 years old was 32%, and the group over 8 was only 22 percent. Bacterial recovery rate was inversely related to the dramatic increase with age of IgA and IgG and lysozyme levels in effusions.
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PMID:Chronic middle ear effusions. Immunochemical and bacteriological investigations. 80 83

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

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

Middle ear adenoma (MEA) is a rare tumor postulated to take origin from the lining epithelium of the middle ear cavity. The authors report on a case of MEA arising in a 53-year old woman suffering from a sensation of fullness in her left ear, otalgia, and light left-sided hearing loss. Histopathologically, the lesion was composed of cuboidal and polygonal cells displaying a trabecular, tubulo-glandular, and solid pattern of growth. Immunohistochemically, neoplastic cells diffusely stained with anti-vimentin antibodies and were focally positive for chromogranin A, neuron-specific enolase, lysozyme, and cytokeratins AE1/AE3. The majority of tumor cells showed weak and diffuse staining with both anti-PP and anti-ACTH antibodies and intense positivity with anti-glucagon and anti Leu-7 antibodies. Ultrastructural investigation revealed both mucinous-glandular and neuroendocrine differentiation. The authors suggest that the appropriate terminology would be adeno-carcinoid or amphicrine tumor of the middle ear rather than "adenoma," a term that does not reflect its dual nature.
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PMID:Middle ear adenoma is an amphicrine tumor: why call it adenoma? 1129 23

Clinicoimmunological, microbiological and cytological examinations were made in 96 patients with otitis media purulenta chronica (OMPC) and otogenic intracranial complications. It was found that in different clinical forms of OMPC nonspecific defense and immunity indices vary. In OMPC and chronic purulent mesotympanitis the indices change insignificantly. In chronic purulent epitympanitis and otogenic intracranial complications there was suppression in T-cell immunity and nonspecific defense. Middle ear secretion contained less SIgA and lysozyme, blood contained more amount of IgA and IgM and less of IgG. Deficiency of general and local defense antiinfectious mechanisms shows significance of immune and nonspecific resistance in transformation of ear inflammation into chronic phase and development of complications. Alterations in immunity, nonspecific defense and tympanic cavity depend on the causative agent of OMPC. Association of St. aureus with gramnegative flora or anaerobic infection cause the greatest immune deficiency. Temporal bone surgery and standard treatment for 21 days fail to eradicate initial immune disorders in the blood and middle ear. Thymalin immunocorrection improves nonspecific defense and immunity, attenuates inflammation and stimulates reparative processes in the trepanation wound of the ear.
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PMID:[Pathogenesis and treatment of chronic purulent otitis media and its complications: immunological aspects]. 1151 39