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)

The destruction of proliferating lymphoid cells within germinal centers with subsequent replacement by histiocytoid cells has been described in infants and children dying of viral and bacterial infections. The etiology and significance of "epithelioid germinal centers" (EGCs) are unknown. The cells implicated in forming EGCs have included histiocytes and dendritic reticulum cells. We have studied four children at autopsy who died at ages ranging from 10 months to 7 years. Three contracted fatal infections, one with fulminant meningococcemia, one with bacterial sepsis, and one with viral hepatitis. The fourth child contracted viral pneumonitis and died of acetaminophen toxicity. Epithelioid germinal centers were found in numerous lymphoid organs (spleen, lymph nodes, and Peyer's patches) in all four cases. Avidin-biotin complex immunohistochemical analysis performed on formalin-fixed splenic tissue from the first three cases and snap-frozen splenic tissue from the second case revealed an absence of B cells in the follicular centers. The mantle zones surrounding follicles were thin but intact. The histiocytoid cells expanding the germinal centers were positive for S100 and R4/23 (dendritic reticulum cells) and negative for numerous histiocyte markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme). Increased numbers of killer cells (Leu-7) were present within the affected germinal centers in the three cases in which material was available for immunohistochemical studies. Overwhelming infections in these patients seem to result in anomalous natural killer cell activation resulting in localized nonselective destruction of follicular centers similar to anomalous natural killer cell activity reported to occur in fatal infectious mononucleosis. This may lead to an acquired immunodeficiency that precludes long-term survival in affected patients.
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PMID:Epithelioid germinal centers in overwhelming childhood infections. The aftermath of nonspecific destruction of follicular B cells by natural killer cells. 284 41

72 patients suffering from recurrent tonsillitis, and ten with infectious mononucleosis were compared by morphological and immunological studies. The distribution of Ig-containing plasma cells (IgA, IgG, IgM), lambda- and kappa-chains, lysozyme and Alpha-1-antitrypsin in tonsils was determined by the unlabelled antibody peroxidase-antiperoxidase method and correlated with the structure of the tonsils (follicles, interfollicular area, and reticular epithelium). While recurrent tonsillitis was associated with slight follicular hyperplasia, infectious mononucleosis was characterised by a marked distortion of the tonsillar architecture, reduction in the number of follicles and a mixed cellular proliferation. The cellular infiltration was composed of small, well differentiated lymphocytes, atypical lymphocytes (Downey cells), plasma cells, immunoblasts, and a variable number of pleomorphic immunoblasts (Reed-Sternberg-like-cells). The binucleated or multinucleated immunoblasts contained IgA, IgG, and IgM. Ig-producing cells occurred in all compartments. In recurrent tonsillitis most were found in the reticular epithelium, but in infectious mononucleosis their density was highest in the interfollicular area. There was a general prominence of IgG cells, confirming that the tonsils resemble lymph nodes more closely than the lymphoid tissue of the alimentary tract. Cells containing lambda and kappa chains were found in all follicle centres and extra-follicular areas. They gave evidence of polyclonality in both diseases. Lysozyme and Alpha-1-antitrypsin were present only in the vessels.
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PMID:[Comparative immunocytochemical studies of recurrent tonsillitis and infectious mononucleosis]. 388 56

Bacterial samples were obtained from the tonsillar surfaces of seven patients (four males, three females; median age 18 years, range 15 to 21 years) suffering from acute infectious mononucleosis with concomitant pharyngotonsillitis, and from five healthy controls. By using gold-labelled antiserum to human lysozyme and lactoferrin, micro-organisms on the tonsillar surfaces coated with these antibacterial substances could be identified by tracing the gold particles in the transmission electron microscope. In healthy individuals, most of the bacteria were coated with lysozyme and significantly more bacteria were coated with lysozyme than with lactoferrin (p < 0.01). In patients there was a non-significant reduction in lysozyme-coating of the bacteria, whereas lactoferrin-coating was significantly increased (p < 0.01). Changes in the lysozyme and/or lactoferrin coating of the tonsillar surface bacteria on the palatine tonsils during infectious mononucleosis cannot explain the tendency to immense local bacterial colonization with commensals and proneness to bacterial penetration into the epithelial cells.
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PMID:Immunocytochemical localization of lysozyme and lactoferrin attached to surface bacteria of the palatine tonsils during infectious mononucleosis. 1194 85