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)

Serum lysozyme (muramidase) concentrations were determined in 55 patients with inflammatory bowel disease, 6 with miscellaneous bowel disease, 40 with pulmonary tuberculosis, and in 20 normal subjects. The mean (+/- SE) lysozyme concentration for each group was as follows: controls 6,95 +/- 0,36 microgram/ml; ulcerative colitis 9,61 +/- 1,02 microgram/ml; inactive Crohn's disease 7,61 +/- 0,53 microgram/ml; active Crohn's disease 20,77 +/- 2,17 microgram/ml; sputum-negative tuberculosis 13,05 +/- 1,06 microgram/ml; and sputum-positive tuberculosis 20,35 +/- 2,08 microgram/ml. The mean enzyme levels were significantly higher in patients with Crohn's disease than in those with ulcerative colitis (P less than 0,05) or in normal controls (P less than 0,01). Our findings suggest that serum lysozyme levels may be useful in differentiating active Crohn's disease from ulcerative colitis, but the results overlap somewhat. However, the enzyme level may be a useful index of disease activity in following up patients with Crohn's disease. As tuberculosis is endemic in this country it must first be excluded, because patients with pulmonary tuberculosis have similarly high levels of serum lysozyme.
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PMID:Serum lysozyme in Crohn's disease and ulcerative colitis. 60 77

Lysozyme in the urine in concentrations greater than 3 micrograms per milligram of creatinine reflects renal tubular disease or dysfunction in patients without bowel disease or leukemia. We therefore used urine lysozyme assays to assess renal response to percutaneous nephrostomy and stone removal in 42 patients. Eight patients had striking increases (4.2-21.1 [mean 7.58] micrograms/mg creatinine) immediately after nephrostomy puncture in urine obtained directly from the punctured kidney. Lysozyme declined sharply thereafter and was within normal limits in all cases by postoperative day 3. This increase appeared to result from bleeding into the urine from the tract. Five other patients had lysozymuria on admission, only 1 of whom had a sharp increase after nephrostomy puncture. In the remaining patients, the lysozyme levels remained within normal limits throughout the hospital course. These data are further evidence of the absence of significant deleterious effects of nephrostomy puncture on the kidney.
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PMID:Impact of percutaneous renal stone removal on renal function: assessment by urinary lysozyme activity. 292 62

Histiocytic ulcerative colitis (HUC) is a chronic enteropathy which most notably occurs in Boxer dogs and French bulldogs. The inflamed mucosa is hallmarked by large, foamy, periodic acid-Schiff (PAS)-positive macrophages infiltrating the colonic mucosa. As little is known about their origin and phenotype, an immunohistochemical study was performed using different macrophage markers. Generally, canine colonic macrophages showed high expression of ionised calcium-binding adaptor molecule 1 and MHC class II. In canine HUC, macrophages revealed up-regulation of lysozyme and L1 Ag but decreased CD163 expression compared with controls, suggesting them to be pro-inflammatory cells, whereas the healthy colonic mucosa was characterised by an anti-inflammatory macrophage phenotype. In addition, PAS reaction was used to discriminate macrophage subpopulations. PAS- macrophages displayed higher expression of L1 Ag and CD64, whereas PAS+ cells, which were only present in HUC patients, were characterised by increased expression of lysozyme, inducible nitric oxide synthase and CD204. This indicates PAS+ cells to be mature macrophages contributing to the inflammatory process, which are most likely maintained by differentiation of immature PAS- macrophages continuously recruited from blood monocytes. In summary, macrophage heterogeneity in canine HUC probably illustrates their different maturation states and functions compared with the healthy animals.
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PMID:Heterogeneity of macrophages in canine histiocytic ulcerative colitis. 2810 85

Congenital tufting enteropathy (CTE) is an autosomal recessive disease characterized by severe intestinal failure in infancy and mutations in the epithelial cell adhesion molecule (EPCAM) gene. Previous studies of CTE in mice expressing mutant EpCAM show neonatal lethality. Hence, to study the cellular, molecular, and physiological alterations that result from EpCAM mutation, a tamoxifen-inducible mutant EpCAM enteroid model has been generated. The presence of mutant EpCAM in the model was confirmed at both mRNA and protein levels. Immunofluorescence microscopy demonstrated the reduced expression of mutant EpCAM. Mutant enteroids had reduced budding potential as well as significantly decreased mRNA expression for epithelial lineage markers (Mucin 2, lysozyme, sucrase-isomaltase), proliferation marker Ki67, and secretory pathway transcription factors (Atoh1, Hnf1b). Significantly decreased numbers of Paneth and goblet cells were confirmed by staining. These findings were correlated with intestinal tissue from CTE patients and the mutant mice model that had significantly fewer Paneth and goblet cells than in healthy counterparts. FITC-dextran studies demonstrated significantly impaired barrier function in monolayers derived from mutant enteroids compared with control monolayers. In conclusion, we have established an ex vivo CTE model. The role of EpCAM in the budding potential, differentiation, and barrier function of enteroids is noted. Our study establishes new facets of EpCAM biology that will aid in understanding the pathophysiology of CTE and role of EpCAM in health and disease.NEW & NOTEWORTHY Here, we develop a novel ex vivo enteroid model for congenital tufting enteropathy (CTE) based on epithelial cell adhesion molecule (EPCAM) gene mutations found in patients. With this model we demonstrate the role of EpCAM in maintaining the functional homeostasis of the intestinal epithelium, including differentiation, proliferation, and barrier integrity. This study further establishes a new direction in EpCAM biology that will help in understanding the detailed pathophysiology of CTE and role of EpCAM.
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PMID:Enteroids expressing a disease-associated mutant of EpCAM are a model for congenital tufting enteropathy. 3143 11