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)

Lysozyme (EC 3.2.1.17) concentrations were measured in the serum and stools of patients with inflammatory bowel disease and compared with the concentrations in similar material from normal controls, patints with non-inflammatory gastrointestinal disease, and patients without gastrointestinal disease. By the turbidometric method, values of lysozyme (microgram/ml +/- SD) are considerably greater in the serum of patients with active Crohn's disease (9.2 +/- 2.7) than in the serum of healthy controls (4.4 +/- 2.0). They do not, however, distinguish individual patients with Crohn's disease from those with ulcerative colitis nor from those with a variety of other gastrointestinal conditions. The lysoplate method gives much higher values for serum lysozyme than the turbidometric method but there is a considerable overlap between the results for patients with Crohn's disease (60.1 +/- 30.7) and normal controls (27.4 +/- 17.5). There is only a moderate correlation between the results given by the two methods (r = 0.56) and it is suggested that factors other than enzyme activity and methodological variation are responsible for the observed differences. This is supported by the finding that, with Crohn's disease in remission, serum lysozyme values (lysoplate) return to normal values but with the turbidometric method remain raised. Mean faecal lysozyme levels, expressed either as a concentration or as total daily excretion, in patients with inflammatory bowel disease are very significantly greater than values in healthy controls and in diseased subjects without diarrhoea but are not significantly different from those subjects with other causes of diarrhoea.
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PMID:Serum and faecal lysozyme in inflammatory bowel disease. 63 44

Serum lysozyme (muramidase) activity was determined by the Lyso-Plate diffusion technic in 419 subjects consisting of normal persons and patients with Crohn's disease, ulcerative colitis, nonspecific diarrhea and various other disorders. Lysozyme activity in the normal subjects did not exceed 37.8 microgram/ml. The values in the several groups of patients overlapped markedly with each other and with the normal range. Approximately two-thirds (62.1%) of the 37 patients with Crohn's disease had values that were within the normal range. In about half (51.8%) of the patients with this disease in whom the process was clinically active, serum lysozyme activity was increased. Of 10 patients with Crohn's disease who had undergone resection, heightened serum lysozyme activity was found only in the three patients in whom there was clinical evidence of recurrence of the disease. It is concluded that serum lysozyme activity is not a dependable means of distinguishing Crohn's disease from ulcerative colitis or nonspecific diarrheas. The determination would appear to be of value, however, in helping to identify activity, recurrence, or extension of the disease in patients with Crohn's disease.
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PMID:The diagnostic value of serum lysozyme activity in inflammatory bowel disease. 91 Jul 87

Non-immunological defence mechanisms represent an important line of intestinal defence in addition to humoral and cellular immunity. This review summarises the evidence for the role of the non-immunological defence system. Protective factors that have been amply documented are gastric juice, intestinal motility, and intestinal flora. Components of pancreatic juice, lysozyme, and epithelial cell turnover may also be involved. Special attention is given to gastric acid, infection with Helicobacter pylori, and hypochlorhydria and their association with infectious diarrhoea. Epidemic hypochlorhydria is discussed since this increases sensitivity to intestinal infections in third world countries.
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PMID:Non-immunological defence mechanisms of the gut. 164 43

Escherichia coli B/SM, strain 1-1, was killed dose dependently by human hereditary C9-deficient serum (C9DHS), which was shown to contain no C9 Ag by an ELISA method. On the other hand, human hereditary C7-deficient serum did not kill the bacteria under similar conditions. The bactericidal activity of C9DHS was inhibited by rabbit anti-C5 antibody but not by murine anti-C9 mAb. The anti-C9 antibody decreased the bactericidal activity of normal human serum (NHS) to the level of that with C9DHS. Sheep anti-human lysozyme antibody did not affect the bactericidal activity of C9DHS or NHS even when added at more than twice the concentration required to block the serum lysozyme activity on Micrococcus luteus. After treatment with C9DHS and washing, surviving Escherichia coli were killed by C9, but not by lysozyme, transferrin, or both. Other strains of E. coli (K12 W3110, C600, and NIHJ) and Salmonella typhimurium (strain NCTC 74), all maintained in the laboratory, were also killed by C9DHS. However, pathogenic strains recently isolated from patients with traveler's diarrhea and some strains of S. typhimurium were resistant to both C9DHS and NHS, at least at the serum concentration tested. A concentration of 0.1 M Tris did not increase the susceptibility of serum-resistant strains of bacteria to C9DHS, but made one strain of S. typhimurium tested susceptible to NHS, but not to C9DHS. These results clearly showed that C9DHS kills bacteria that are sensitive to NHS through activation of C up to the step of C8 in the same way that C9-deficient C serum lyzed sensitized erythrocytes.
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PMID:Bactericidal activity of C9-deficient human serum. 173 Aug 76

A simple and economical method was developed for using biotinylated DNA probes to hybridize with bacterial colonies belonging to the various categories of diarrhea-causing Escherichia coli. Simplification and cost containment were achieved by using Whatman no. 541 filter papers instead of nitrocellulose, by minimizing the concentration of proteinase K (an expensive but necessary reagent used to pretreat the colony blots prior to hybridization with biotin-labeled DNA probes) and by reusing hybridization solution containing labeled probe DNA. After exposing the colony blots to lysing solution and steam, followed by lysozyme (1.5 mg/ml), sucrose (25%), and proteinase K (10 micrograms/ml) treatments, biotinylated probes were used to detect enterotoxigenic, enteropathogenic, enterohemorrhagic, diffuse adherence, and enteroinvasive categories of diarrhea-causing E. coli with a high level of sensitivity and specificity. Three independent observers who were experienced in reading DNA blots recorded remarkably similar results, while less satisfactory results were obtained when the blots were read by an inexperienced observer. This technique will be useful in laboratories in which radioactive isotopes are unavailable or impractical and in which budgets are restricted.
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PMID:Practical and economical method for using biotinylated DNA probes with bacterial colony blots to identify diarrhea-causing Escherichia coli. 225 25

The purpose of this work was to investigate the relationship between rotavirus infection, diagnosed in faeces using the serological test, in calves with diarrhoea and the activity of lysozyme, alpha-amylase, lipase and trypsin in the same material. The faeces were taken from 28 sick and 1 healthy animals, aged from 1 to 5 days, for microbiological and enzymatic examination. No correlation was found between lysozyme activity in faeces and rotavirus infection. Similar results were obtained with the other enzymes.
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PMID:Rotavirus infection in newborn calves. I. Evaluation trials of certain enzymes in faeces. 246 66

In food toxinfections caused by various microorganisms (Staphylococcus, Escherichia, Klebsiella, Proteus, Citrobacter, etc.) a decrease of lysozyme debit and an increase of pH of gastric juice were found. One third of patients exhibited lactose deficiency of the small intestine. Treatment with furazolidone contributed to the development of lactase deficit and delayed stools normalization. Crystalline lysozyme shortened duration of febrile reaction and diarrhea, its intake facilitated lactose hydrolysis.
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PMID:[Clinico-pathogenetic basis for using crystalline lysozyme in the combined therapy of food toxinfections]. 381 53

There were several problems with the editorial on breastmilk and infection appearing in the May 30 Lancet. Of the antiinfective substances in human milk, lysozyme was omitted, as were the bifidus factor, the antistaphylococcus factor, antitoxins for neutralizing Vibrio cholerae and Escherichia coli, lactoperoxidase, and volatile fatty acids. Low pH and the exclusive specific bifidus bowel flora are all components of the same interacting antiinfective screen, as are macrophages and lymphocytes. Secretory IgA in breastmilk as a developmental bridging mechanism until the infant's intestine can secrete IgA itself at 3 months, is not recognized. The protective effect of human milk against death from diarrheal disease is well-known both in Europe and North America and in such disadvantaged communities as exist in the 3rd world. Clearly, this is related in part to a lack of contamination of human milk; the process is both passive and active. Recent studies show protective effects against infectious episodes in babies in well-to-do communities. The role of colostrum as an immunological bolus for the newborn is barely mentioned despite long known high levels of antibodies and the probability that neonatal diarrhea is often a colostrum deficiency syndrome. Doses of colostrum (5 mg/kg daily) reduce the incidence of endemic nursery neonatal E. coli diarrhea. The protective effects extend to other extraintestinal infections and to certain viral infections. There is no mention of the dyadic immunological interaction between mother and young baby, particularly through the proven "gut-mammary axis". The editorial concludes by damning with faint praise. For example, it is outdated, negative editorial revealing scant knowledge of the considerable published literature which documents the protective effect of breastfeeding against many alimentary and extraintestinal infections.
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PMID:Breast milk and infection. 611 83

The effects of season and variations in the prevalence of infectious disease on the concentrations and daily production of breast-milk immunoproteins were studied in 152 rural Gambian mothers and their children up to 26 months post-partum. IgA, IgG, IgM, C3, C4, lactoferrin, lysozyme and secretory component concentrations and breast-milk volumes were measured longitudinally over a six month period which encompassed dry and rainy seasons. No increase in the production of any immunoprotein was observed at the time of maximum prevalence of serious infectious diseases, especially diarrhoea, in the children. Enhanced secretion of certain immunoproteins was noted in mothers of children aged 9-18 months at the beginning of the rainy season. There was some evidence that this may have been associated with skin sepsis, particularly impetigo, in the children. The production of most immunoproteins fell during the rainy season. This was not the result of declining maternal food intakes as similar decreases were seen for women receiving a dietary supplement.
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PMID:Breast-milk antimicrobial factors of rural Gambian mothers. II. Influence of season and prevalence of infection. 654 89

Morphological abnormalities in Paneth cells occur in patients with acrodermatitis enteropathica, a hereditary disease associated with zinc deficiency; furthermore, rat Paneth cells contain large amounts of zinc. This study was conducted to assess the effect of severe zinc deficiency in Sprague-Dawley rats on various parameters of Paneth cells. Morphology at both the light microscopical and ultrastructural levels, Paneth cell numbers per crypt and the intracellular distribution of lysozyme were not altered by zinc deficiency. A weak correlation (r = +0.38, P = 0.05) was noted between ileal zinc concentration and numbers of IgA-containing Paneth cells per crypt. These findings indicate that the morphological abnormalities noted in human Paneth cells in patients with acrodermatitis enteropathica cannot be reproduced by experimental severe zinc deficiency in rats. Furthermore, these generally negative findings suggest that the severe diarrhoea often associated with zinc deficiency is not attributable to abnormalities induced in Paneth cells by zinc deficiency.
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PMID:Ileal Paneth cells and IgA system in rats with severe zinc deficiency: an immunohistochemical and morphological study. 744 Feb 49


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