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)

Histochemical and immunohistochemical studies performed in only a few cases of sinus histiocytosis with massive lymphoadenopathy (SHML) indicated that SHML cells belong to the macrophage--histiocyte system, though their exact origin is still uncertain. We analyzed the morphological, antigenic and enzymatic characteristics of the histiocyte-like cells in one paediatric case of SHML (also named Rosai-Dorfman disease). The SHML cells expressed the S-100 protein, lectins concanavalin A, peanut agglutinin and monocyte-macrophage related antigens CD 11c, CD 14, CD 33, CD 68 and LN 5. Reactivity with other anti-macrophage antibodies (MAC387, lysozyme, alpha-1 anti-chymotrypsin) was variable. The CD1a antigen was present only in scattered cells, whereas HLA-DR and the HLA-DR associated invariant chain were absent. Cytochemistry demonstrated an intense activity of acid phosphatase and non specific esterase of SHML cells. A large amount of medium sized mononuclear cells were located in the sinuses and intersinusoidal tissue. Our findings suggest that SHML cells have intermediate features between phagocytes and Langerhans cells/interdigitating reticulum cells. The heterogeneity of marker expression on SHML cells might be related to the local content of factors (e.g., cytokines), capable of modulating the phenotype of monocyted and derived cells.
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PMID:Sinus histiocytosis with massive lymphoadenopathy (Rosai-Dorfman disease). Clinico-pathological analysis of a paediatric case. 840 78

Little is known about the nature of the large intrasinusoidal cells exhibiting cytophagocytosis, which are the histologic hallmark of sinus histiocytosis with massive lymphadenopathy (SHML) (Rosai-Dorfman disease). Using a broad panel of monoclonal and polyclonal antibodies, we analyzed the immunophenotype of the cell infiltrates in seven lymph node biopsy specimens from five cases of SHML. The SHML cells constantly expressed the S-100 protein, concanavalin agglutinin and peanut agglutinin lectins, and monocyte-macrophage-associated antigens CD 11c, CD 14, CD 33, CD 68, and LN 5. Labeling with other antimacrophage antibodies was extremely variable, with some (MAC 387, lysozyme) restricted to clusters of SHML cells and others (CD11b, CD 36, alpha-1-antichymotrypsin) staining only scattered cells. The CD 1a antigen was found on some cells in only one case, whereas HLA-DR and the HLA-DR-associated invariant chains were absent. The heterogeneity of SHML cell marker expression might be related to the local content of factors (eg, cytokines) capable of modulating the phenotype of monocytes and derived cells. All cases presented with huge amounts of medium-sized mononuclear cells accumulated in the sinuses and intersinusoidal tissue. These cells expressed the S-100-/CD 11b+/CD 11c+/CD 14+/CD 16+/CD 33+/CD 36+/lysozyme+/MAC 387+/HLA-DR+ phenotype. These recently immigrated monocytes might represent the immediate precursors of SHML cells.
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PMID:Immunophenotypic characterization of the cell infiltrate in five cases of sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease). 159 87

Alveolar macrophage function was studied immunocytochemically using three monoclonal antibodies--macrophage CD 68 KP 1 (M), protein CD 11C (P), and anti-elastin (EL)--and three polyclonal antibodies--lysozyme (LZ), alpha-1-antitrypsin (AAT), and alpha-1-antichymotrypsin (AACT). The material for study was smears obtained from bronchial washings from 15 healthy persons and 60 patients with respiratory infections or primary or secondary malignant lung infiltration. Eight of the healthy group and 40 of the patient group were smokers (SM). The percentage of cells obtained from the washings which were macrophages was also measured. The intensity of staining reactions for each of the six antigens was noted and in general more intense staining was noted in smokers than in non-smokers. More intense staining was observed in patients with pulmonary infections (group II PI) and metastatic pulmonary infiltrations (group IV MP Ca) than in controls (group IC), while patients with primary lung cancer (group III PP Ca) had highly reduced staining reactions. The number of macrophages was similarly increased in all groups in comparison with the IC group for non-smokers and in all groups except III PP Ca for smokers. It is concluded that smoking, pulmonary infections, and metastatic infiltration of the lung are associated with an increase in the number and activity of alveolar macrophages, while patients with primary lung cancer have an increase in the number of macrophages which are functionally incompetent.
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PMID:Antigen expression of alveolar macrophages in smokers and patients with lung diseases. 778 44

Quantitative analysis of lysozyme- and CD68-positive Kupffer cells was carried out in connection with diethylnitrosamine-induced hepatocarcinogenesis in non-human primates. The number of Kupffer cells/mm2 was determined in 28 cases of hepatocellular carcinoma (HCC) and seven age-matched controls. The Kupffer cell counts (mean +/-SEM) gradually decreased in the following order, irrespective of the histochemical markers (lysozyme or CD 68) used: healthy control liver (101.7 +/- 13.5 and 103.2 +/- 11.9 respectively), non-cirrhotic and non-neoplastic host liver (54.3 +/- 13.6 and 50.5 +/- 15.4), cirrhotic host liver (26.2 +/- 8.2 and 27.2 +/- 3.3), HCC tissue (20.7 +/- 4.4 and 19.3 +/- 4.1) and metastatic foci in the lung (9.8 +/- 1.8 and 9.7 +/- 2.8). The difference between the normal liver and the non-neoplastic, non-cirrhotic portions of the HCC-bearing liver was significant (P < 0.05). A highly significant difference was found between the number of Kupffer cells found in healthy control or non-neoplastic liver and those found in HCC nodules (P < 0.0001 and P < 0.0005 respectively). The results obtained by hematoxylin and eosin staining and lysozyme/CD68 immunohistochemistry were highly similar, indicating that this decrease was attributable primarily to numeric loss of Kupffer cells. The results suggest that the reduction in the number of Kupffer cells in HCC is a constant feature of hepatocarcinogenesis not only in rodent models, but also in non-human primates.
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PMID:Quantitative evaluation of lysozyme- and CD68-positive Kupffer cells in diethylnitrosamine-induced hepatocellular carcinomas in monkeys. 860 89

Malacoplakia, an inflammatory disease characterized by accumulations of phagocytic macrophages, occurs primarily in immunocompromised individuals. Cutaneous involvement is rare. Two men, each with a renal allograft, had expanding nodules on the temple and perianal area (case 1) and perianal, inguinal, and scrotal skin (case 2). Lesions resolved after combined surgical and antibiotic therapy. Histopathologic examination showed dense infiltration with large phagocytic macrophages containing round, concentric, laminar Von Kossa stain-positive inclusion bodies. Histiocytes had positive results for CD 68, lysozyme, and alpha 1-antitrypsin. Electron microscopic examination demonstrated rare intracytoplasmic inclusion bodies with concentric electron-dense laminations of calcium (Michaelis-Gutmann bodies.) Cutaneous malacoplakia should be considered in the differential diagnosis of nodules or draining ulcers, particularly in immunocompromised patients. Because Michaelis-Gutmann bodies are difficult to identify, specimens should be evaluated for cutaneous malacoplakia by immunohistochemical or electron microscopic means.
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PMID:Cutaneous malacoplakia: a report of two cases and review of the literature. 865 20

By clinical, pathologic and immunohistochemical study on aniomatoid malignant fibrous histiocytoma, which is a relatively uncommon soft tissue tumor described by Enzinger in 1979, and often misdiagnosed, we are reporting 32 cases of this lesion. The distinctive histopathology were: (1) Cystic change filled with hemorrhagic fluid or blood, (2) surrounded by nests of fibroblastlike and histocyte-like cells and (3) intermingled with chronic inflammatory cells, (4) often surrounded by a fibrous pseudocapsule. Immunohistochemical staining done in 4 cases showed all to be positive in lysozyme, three positive in Mac 387 and CD 68. These results support their histiocytic origin. Follow-up information was available in 25 of 32 cases. All the 25 patients were alive, 4 with recurrence (16%), 1 with metastasis (4%). These results concur with the opinion that intrinsically, this is a low grade tumor.
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PMID:[Angiomatoid malignant fibrous histiocytoma]. 876 38

A case of primary splenic angiosarcoma with involvement of two accessory spleens is presented. The tumor cells are immunoreactive for endothelial markers (CD 31, CD 34, factor VIII associated antigen) and express also histiocytic antigens (CD 68, lysozyme, Cat-hepsin D, alpha-1-antitrypsin, alpha-1-anti-chymotrypsin) as well as CD 8. This marker profile suggests that the presented angio-sarcoma originates from sinus cells with histiocytic and endothelial differentiation and may be regarded as the malignant variant of littoral cells angioma.
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PMID:[Littoral cell angiosarcoma of the spleen. Morphologic, immunohistochemical findings and consideration of histogenesis of a rare splenic tumor]. 943 77

The role of macrophages in the killing and elimination of microfilariae (mf) was studied immunohistologically in 14 lymph nodes from 10 patients with generalized onchocerciasis 20-68 h after treatment with a single oral dose of 150 microg/kg ivermectin. Mf with signs of damage at light microscopical level were surrounded by a cellular infiltrate comprising macrophages, eosinophils and neutrophils, whereas light microscopically intact mf mostly showed no cellular reaction. Resident mature macrophages expressing the CD 68 epitope usually neither migrated nor attached to damaged mf, especially on the first and second day after ivermectin treatment. However, many young invading macrophages labelled for the L1 protein (antibodies 27 E 10, MAC 387, S 36.48 and 8.5C2) were found within the cellular infiltrate around damaged mf and in adherence to the mf in all lymph nodes after ivermectin treatment. Free L1 protein was observed on the cuticle of the mf. The attacking macrophages contained increased amounts of the enzymes lysozyme, alpha-1-antichymotrypsin and alpha-1-antitrypsin compared to resident macrophages. Free enzymes were found on the cuticle of the mf and around them, indicating a role of these enzymes in the inflammatory reaction to the parasites. The attacking macrophages were strongly labelled for human HLA-DR and they showed further an increased expression of the complement receptors CR1 (CD 35) for C3b and CR3 (CD 11b) for C3 bi in comparison to resident macrophages and thus were considered as activated macrophages. Rarely fragments of mf were seen within multinuclear macrophages. We conclude that young activated macrophages play a major role in the elimination of mf transported to the regional lymph nodes after ivermectin treatment. The immunohistological findings are in accordance with the assumption that these activated macrophages together with granulocytes contribute to the killing of the damaged mf. They also help to limit the damage of the host tissue by release of alpha-1-antichymotrypsin and alpha-1-antitrypsin.
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PMID:Immunohistological studies on macrophages in lymph nodes of onchocerciasis patients after treatment with ivermectin. 943 72

We present a case of leukemia cutis associated with a prominent giant cell component. This lesion was initially diagnosed as chronic granulomatous inflammation 1 year before the definitive diagnosis of leukemia cutis was made. Skin biopsy specimens showed numerous Langhans-type giant cells occurring singly and as poorly formed granulomas. However, the majority of the infiltrate consisted of immature myeloid cells, positive for chloroacetate esterase, lysozyme, and CD 68. Subsequent peripheral blood and bone marrow examinations confirmed the progression of the disease to acute myeloid leukemia.
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PMID:Leukemia cutis with prominent giant cell reaction. 950 69

Lysozyme is an innate non-immunologic antibacterial enzyme produced by the Paneth cells of the upper intestinal tract. Lysozyme is not normally secreted in the lower intestinal tract. Previous reports indicate, however, that lysozyme may be secreted by colorectal neoplasias. The aim was to audit lysozyme expression in colorectal diseases including neoplasias. For that purpose, sections were stained with lysozyme (Muramidase), Ki67 (MIB1) and CD 68. Intense lysozyme overexpression (+++) was compared among 177 colorectal tissues: 35 having normal mucosa, 20 regenerative mucosa in inflammatory bowel disease (IBD), 2 inflammatory polyps, 3 collagenous colitis, 2 melanosis coli, 21 hyperplastic polyps, 42 tubular adenomas, 9 serrated adenomas, 30 villous adenomas and 13 invasive carcinomas. Intense lysozyme overexpression (+++) was found in 9.5% of the hyperplastic polyps, in 97.6% of the tubular adenomas, in 88.9% of the serrated adenomas, in 93.3% of the villous adenomas, in 76.9% of the carcinomas, but in none of the other tissues investigated. Neoplastic colorectal cells may acquire the capacity to produce lysozyme. The presence of that enzyme may not be a haphazard, capricious event in mutated colorectal epithelial cells but part of a more elaborate molecular behavior, not necessarily antibacterial. Recently, it was demonstrated that patients having lysozyme-secreting breast carcinomas were associated with a favorable prognosis. Whether lysozyme expression has any bearing on the biological behavior of colorectal carcinomas remains to be elucidated. Lysozyme overexpression (+++) also occurred in 2 of the 21 hyperplastic polyps, suggesting that intense lysozyme production might herald a possible dysplastic evolution in some hyperplastic polyps.
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PMID:Colorectal adenomas produce lysozyme. 1498 84


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