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 mouse sensitized by subcutaneous (sc) injection of lysozyme in emulsion of Freund's complete adjuvant (FCA) was shown by a modified footpad test to develop three kinds of hypersensitivities. Injecting lysozyme in 2.5-mul emulsion of Freund's incomplete adjuvant (FIA) into the footpad elicited strong footpad swelling in 30 min (anaphylactic reaction), in 3 hr (Arthus-type reaction) and in 24 hr (delayed-type hypersensitivity; DTH). The mice showing anaphylactic reaction in the footpad test manifested severe active systemic anaphylaxis, and the sera of these animals showed high IgG1 antibody titers with only sparingly detectable or no IgE antibody titers. In the sensitizing system with the use of FCA, the antigenicity of S-carboxymethylated lysozyme (CM-lysozyme) devoid of the three-dimensional conformation of lysozyme was compared with that of the native molecule. CM-lysozyme and lysozyme completely cross-reacted to each other in DTH, but not at all in the anaphylactic or Arthus-type reaction or in IgG1 antibody production. CM-lysozyme was shown also to have the ability to bestow immunological memory for the induction of humoral immunity against lysozyme; intravenous (iv) injection of lysozyme in saline or sc injection of CM-lysozyme-FCA alone failed to induce immediate hypersensitivities and IgG1 antibody production against lysozyme, but pre-sensitization by sc injection of CM-lysozyme-FCA enabled the animal to induce these responses to significant levels when iv injection of lysozyme in saline was given as a booster.
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PMID:Cell-mediated and humoral immunity in mice: cross reaction between lysozyme and S-carboxymethylated lysozyme studied by a modified footpad test. 5 Nov 9

Human duodenal, jejunal, and ileal samples obtained at necropsy and by peroral and surgical biopsy, were studied by light microscopy using the unlabelled antibody enzyme method for imunocytochemical staining of lysozyme and immunoglobulins. Paneth cells contained IgA and IgG, but not IgD IgE, or IgM. Staining intensity indicated that IgA and IgG were present in amounts greater than in other epithelial cells. There was pronounced variation in the immunoglobulin content of Paneth cells. Rat Paneth cell containing IgA and lysozyme and are capable of the phagocytosis and degradation of microorganisms. These observations suggest that human Paneth cells may have similar functional capabilities.
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PMID:Immunoglobulins within human small-intestinal Paneth cells. 5 40

Among 998 children with recurrent respiratory diseases 26 children with selective IgA deficiency were found. Three groups were considered according to IgA level in serum: group I with IgA under 0.05 g per litre; group II with IgA between 0.05 and 0.3 g per litre; group III with IgA above 0.3 and under 1 g per litre. Non specific immunity was studied in these patients including immunoglobulin levels, alpha-1-antitrypsin (A.A.T.) phenotypes, phagocytosis of staphylococcus aureus by PMN, lysozyme level, complement system. Cellular immunity was evaluated by IDR tests and rosette forming cells (RE). Only non specific immune systems were disturbed in some patients and appeared as aggravating factors in IgA deficient patients. We found: Abnormal phenotypes of ATT in 11 cases; deficiencies of engulfment in 6 cases, of bactericidal activities of PMN in 7 cases out of 16 studied; decrease of lysozyme level in 4 cases out of 17 studied; increase of IgE level in 9 cases with atopic symptoms in 7 patients. In our experience the chief aggravating factor in IgA deficient patients is abnormal phenotype of AAT.
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PMID:[Non specific immunity of children with selective IgA deficiency. Aggravating role of abnormal phenotype of alpha-1-antitrypsin (author's transl)]. 31 58

Seven patients (6 with connective tissue diseases, 1 with bronchial asthma) have been studied before, during, and after prednisone therapy. Maximum dose was 15 mg daily, which was tapered off to zero within three months. All patients showed striking subjective improvement during therapy. The ESR reflected this improvement but the acute phase proteins did not. The serum concentration of prealbumin rose significantly during the period of most intensive steroid treatment. IgE decreased in the patient with bronchial asthma, but otherwise the immunoglobulins did not change, and positive serological tests remained unchanged. Contact sensitization to haptens was induced without impairment during therapy. Prednisone induced rises in blood lymphocyte and neutrophil concentrations. Lymphocyte transformation, both mitogen- and antigen-induced, was not influenced by therapy, but PPD-induced inhibition of leucocyte migration decreased. Neutrophil phagocytosis was unimparied, but bactericidal capacity, stimulated nitroblue tetrazolium reduction, and neutrophil and plasma lysozyme concentrations were all depressed during treatment with prednisone.
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PMID:Sequential studies of lymphocytes, neutrophils and serum proteins during prednisone treatment. 108 10

IL-8 and its structural analogs derived from blood platelets have been proposed as stimuli of IgE-independent basophil activation. In order to clarify the mechanism of action of these peptides, we examined the effects of pure IL-8, connective tissue-activating peptide III (CTAP-III), neutrophil-activating peptide 2 (NAP-2), and platelet factor 4 (PF-4) on blood basophils with and without pretreatment by IL-3, which modulates mediator release. After pretreatment with IL-3, significant histamine release was observed with 10(-8) M and 10(-7) M IL-8 and 10(-7) M NAP-2, but not with the other peptides. At higher concentrations (10(-6) M), however, all IL-8 analogs, as well as the unrelated cationic peptides poly-D-lysine, histone VS, and lysozyme, induced histamine release to variable degrees. Binding and competition studies with [125I]IL-8 revealed specific IL-8R on basophils from a patient with chronic myelogenous leukemia and normal individuals. From 3500 to 9600 receptors with a mean Kd value of 0.15 nM were found on average per chronic myelogenous leukemia and normal basophil, respectively. NAP-2 weakly competed for IL-8 binding. IL-8 and, to a lesser extent, NAP-2 led to a transient rise of cytosolic free calcium concentration ([Ca2+]i), which was independent of a preexposure to IL-3. IL-8 prevented the [Ca2+]i rise induced by NAP-2, but did not influence [Ca2+]i responses to other agonists, e.g. C5a, C3a, or platelet-activating factor. IL-8 induced [Ca2+]i changes and histamine release in IL-3-primed basophils were pertussis toxin sensitive. CTAP-III or PF-4 did not compete for IL-8 binding, did not induce [Ca2+]i changes, and did not influence the [Ca2+]i response to IL-8 and NAP-2. This study shows that IL-8 and NAP-2 activate human basophils by a receptor-mediated mechanism similar to that operating in neutrophils. At high concentrations histamine release can also be induced by cationic peptides by a mechanism that does not involve the IL-8R, and probably depends on cationic interactions.
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PMID:Activation of human basophils through the IL-8 receptor. 138 21

Clinical manifestations were observed only 16 out of 61 patients aged 15-32 years who had hymenolepiasis. Despite their degree, there was impaired dexylose absorption, lower serum lysozyme activity and higher serum complement activity, depressed immunological reactivity parameters (the count of T- and B-lymphocytes, their functional activity), decreased IgA titer and increased IgE titer in the sera in all the patients observed. Six months after the effective dehelminthization, varying immunodepression still remained in all the convalescents. There types of restoration of immunological reactivity were identified: torpid, reactive and highly reactive. The torpid type was significantly more frequently observed in patients with subclinical (asymptomatic) hymenolepiasis course than in patients with its clinical manifestation.
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PMID:[The clinico-immunological characteristics of hymenolepiasis]. 143 57

Seven patients who received a lysozyme, nystatin, and tetracycline containing vaginal suppository because of suspected vaginal infection, developed local or systemic allergic reactions. The coincidence of the symptoms with the repeated use of the suppository as well as skin and lymphocyte transformation tests indicated that the lysozyme in the suppository was responsible for the allergic reactions. This lysozyme preparation contained additional egg proteins, which contributed to the allergic reaction in certain patients: three patients with a previous history of egg allergy and serologic and/or skin test evidence for egg-white sensitization developed the allergic reaction after the first suppository. Four patients had urticaria or anaphylaxis after treatment for at least three days; none of these four patients developed egg allergy. Five of seven individuals had positive skin tests (prick or scratch) to ovomucoid and lysozyme, but none of the patients had lysozyme-specific IgE in the circulation. All seven patients, with or without egg allergy, showed vigorous T cell responses to purified lysozyme and partly to other egg-white proteins in the lymphocyte transformation test, which was absent in controls. Vaginal suppositories that contain lysozyme and other contaminating egg white proteins can either elicit allergic reactions in patients with a preexisting egg white allergy or induce sensitization to lysozyme and other egg white components.
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PMID:Allergy to lysozyme/egg white-containing vaginal suppositories. 147 86

In the present study, 14 cases of Kimura's disease were clinicopathologically studied. The disease occurred at ages ranging from 5 to 75 years. The average age was 37.8 years. Sexes were about equally affected. The most common sites were the subcutis of head and neck, and parotid gland. Simultaneous involvement of lymph nodes occurred in 5 cases. Laboratory findings revealed eosinophilia in almost all the patients, but serum IgE levels were not elevated in 2 patients. Lesions were surgically removed and the clinical course thereafter was favorable for all but one case. Histologically, lesions were characterized by lymphoid follicles, granulation tissue with infiltration by many eosinophils, lymphocytes, plasma cells, mast cells and histiocytes, proliferation of blood vessels and fibrosis. Immunohistochemically, IgE reacted strongly in germinal centers, showing a reticular pattern. IgG-, IgA- and lysozyme-positive cells were scattered mainly in interfollicular granulomatous areas. Pathogenesis of this disease is briefly discussed.
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PMID:Kimura's disease: clinical, histological and immunohistochemical studies. 148 39

Giant papillary conjunctivitis (GPC) associated with contact lens wear is believed to result from an irritative or allergic response to accumulated lens surface deposits. In a masked study, contact lenses worn short-term (2 weeks or less) or long-term (2-12 months), and obtained from patients with and without active GPC, were examined for deposited proteins: IgA, IgE, IgG, IgM, lactoferrin, and lysozyme. Using immunohistochemical methods lenses were separately graded on a 4+ scale for extent of protein coverage. All lenses showed substantial deposits (averaging 50-75% lens coverage) of the normal tear proteins, with the exception of IgE which averaged less than 25% lens coverage; maximum protein deposition was apparent on lenses worn for only 3 days. Both symptomatic and asymptomatic persons deposited similar amounts of the common tear proteins on their contact lenses, with the exception of IgM. A statistically significant increase in IgM deposition was found when the short-term GPC lenses were compared to short-term asymptomatic lenses. Our data suggest that the development of GPC does not depend on amount of deposition of the normal tear proteins IgA, IgG, IgE, lactoferrin or lysozyme. Differences observed in IgM deposition may reflect an immune response in GPC.
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PMID:Evaluation of tear protein deposits on contact lenses from patients with and without giant papillary conjunctivitis. 149 18

The knowledge about the differentiation of basophilic leukocytes is fragmentary. This report discusses a detailed phenotypic characterization of molecular markers for hematopoietic differentiation in a basophilic leukemia cell line, KU812. The expression of markers for lymphoid, erythroid, neutrophil, eosinophil, monocytic, megakaryocytic, mast cell and basophil differentiation was analyzed at the mRNA level by Northern blots in the KU812 cells, and for reference, in a panel of human cell lines representative of the different hematopoietic differentiation lineages. KU812 was found to express a number of mast cell and basophil-related proteins, i.e. mast cell tryptase, mast cell carboxypeptidase A, high-affinity immunoglobulin (IgE) receptor alpha and gamma chains and the core protein for heparin and chondroitin sulphate synthesis. We found no expression of a number of monocyte/-macrophage or neutrophil leukocyte markers except for lysozyme. From earlier studies, it has been shown that lysozyme is not expressed in murine mucosal mast cell lines. This finding, together with the expression of the mast cell carboxypeptidase in KU812 might distinguish the phenotype of this cell line from that typical of mucosal mast cell lines in rodents. We found a low level of expression of the eosinophil and basophil marker, major basic protein, which might indicate a relationship between basophils and eosinophils. No expression is, however, detected with the eosinophil-specific markers eosinophil cationic protein, eosinophil-derived neurotoxin or eosinophil peroxidase. We also report an extensive screening for inducers of basophilic differentiation of the KU812 cells. The most efficient protocol of induction included serum starvation which led to a dramatic increase in a number of markers specific for mast cells and basophils such as tryptase, carboxypeptidase A and the heparin core protein. Finally, diisopropylfluorophosphate analysis of total protein extracts from KU812 show four labeled protein bands with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, indicating that this cell line expresses at least three previously undescribed serine proteases of which one or more could be a potential basophil-specific marker(s).
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PMID:Phenotypic characterization of KU812, a cell line identified as an immature human basophilic leukocyte. 163 3


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