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 distribution of ferritin and lysozyme in 19 normal and abnormal duodenal biopsies was studied by an immunoperoxidase technique. The abnormal biopsies included cases of chronic duodenitis with gastric metaplasia, gastric heterotopia, villous atrophy, and a case of hemochromatosis. Ferritin is demonstrated in duodenal absorptive cells, with the staining being most intense in the hemochromatosis case. It was absent in duodenal cells showing gastric metaplasia and in the surface epithelial cells of most biopsies with villous atrophy and gastric heterotopia. Lysozyme-positive mononuclear inflammatory cells were markedly increased in all abnormal biopsies. Not all lysozyme-positive cells were ferritin positive. The latter were especially abundant in areas with gastric metaplasia. It is suggested that this abundance may be related to passive diffusion of intestinal contents, particularly iron, through the metaplastic areas, and consequently there may be a relationship between the presence of duodenal gastric metaplasia and uncontrolled iron absorption.
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PMID:Ferritin and lysozyme distribution in normal and abnormal duodenal mucosae. 389 Dec 62

In 158 patients with symptoms of non ulcerative dyspepsia, endoscopic, histologic and immunohystochemical studies were performed over three years with the aim of investigating the immunological involvement in the Chronic non specific Duodenitis (CND). After excluding 112 patients with associated pathologies of those not fulfilling technics requisites, a population of 46 subjects was selected and subsequently it was subdivided into four groups. A group of 15 patients with histologically normal duodeno served as control; the rest (31 patients) were grouped according to duodenal compromise into three groups of minor-major severity; Grade 1 (n=12); Grade 2 (n=12); Grade 3 (n=7). The number of immunoglobuline producing cells by mn2 of mucosal area and semiquantitative evaluation of mononucleated cells with cytoplasmatic activity to hydrolitic enzymes (lysozyme or muramidase) were compared among the 4 sub-groups. It was observed a variation in the immunoglobulines rate among controls (IgA: M: G=82, 52: 11, 01: 6,45) regarding the most severe degree (61, 56: 27,30: 11,14). The increase of IgMy G compared with controls was highly significant (p is less than 0.001) and it was noted a correlative IgA diminution. The contribution of hydrolitic enzymes through the presence of "activated" histiocytes was maximal in the most degree-coinciding with the increase of IgM and IgG. This findings indicated that a marked local activation of the Immunitary System type B is observed in the Chronic Nonspecific Duodenitis and its increment, expressed as quali-quantitative variations of the different immunologlobulines and muramidase producing cells, should have lythic activity in the highest degrees. We conclude, proposing this disease as a model of immunological aggression which affects bulbar mucosae.
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PMID:[Evaluation of Ig and muramidase (lysozyme) in unspecified chronic duodenitis (bulbitis)]. 639 Oct 60

Lysozyme is as an innate enzyme with potent antibacterial properties found in Paneth cells in normal duodenal crypts. Since celiac disease concurs with an abnormal duodenal microbiota we explored the expression of lysozyme in this disease. Fifty-three duodenal biopsies were stained with anti-lysozyme: 15 had normal duodenal mucosa (NDM), 7 chronic active duodenitis (CAD), 3 borderline (BL), 17 subtotal villous atrophy (SVA) and 11 total villous atrophy (TVA). NDM showed lysozyme-positive Paneth cells arranged in "Indian file" in 93.3%. In contrast, lysozyme-positive mucus metaplasia in crypts (LPMMC) replacing Paneth cells was found in 71.5% in CAD, in 96.4% in SVA/TVA, and in 2 cases with B. In 19.3% cases with BL/SVA/TVA, LPMMC replaced all Paneth cells in all crypts in entire sections. In crypts and villi, lysozyme-positive goblet cells (LPGC) were found in 92.8%. Changes were more frequent in the duodenal bulb than in pars descendens. In normal duodenal mucosa, absorptive enterocytes and goblet cells migrate from stem cells upwards, while Paneth cells migrate downwards, towards the base of the crypts. In celiac disease stem cells seem to have been re-programmed, as the normal production of Paneth cells in the crypts was replaced by lysozyme-producing mucus cells. LPMMC and LPGC in celiac disease might mirror an antimicrobial adaptation of stem cells to signals generated by pathogenic duodenal bacteria. The molecular mechanism(s) behind the abrogation of Paneth cells in duodenal crypts and its substitution by LPMMC in celiac disease remains to be elucidated.
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PMID:Lysozyme-rich mucus metaplasia in duodenal crypts supersedes Paneth cells in celiac disease. 2176 18

The cells that line the mucosa of the human gastrointestinal tract (GI, that is, oral cavity, oesophagus, stomach, small intestine, large intestine, and rectum) are constantly challenged by adverse micro-environmental factors, such as different pH, enzymes, and bacterial flora. With exception of the oral cavity, these microenvironments also contain remnant cocktails of secreted enzymes and bacteria from upper organs along the tract. The density of the GI bacteria varies, from 103/mL near the gastric outlet, to 1010/mL at the ileocecal valve, to 1011 to 1012/mL in the colon. The total microbial population (ca. 1014) exceeds the total number of cells in the tract. It is, therefore, remarkable that despite the prima facie inauspicious mixture of harmful secretions and bacteria, the normal GI mucosa retains a healthy state of cell renewal. To counteract the hostile microenvironment, the GI epithelia react by speeding cell exfoliation (the GI mucosa has a turnover time of two to three days), by increasing peristalsis, by eliminating bacteria through secretion of plasma cell-immunoglobulins and by increasing production of natural antibacterial compounds, such as defensin-5 and lysozyme. Only recently, lysozyme was found up-regulated in Barrett's oesophagitis, chronic gastritis, gluten-induced atrophic duodenitis (coeliac disease), collagenous colitis, lymphocytic colitis, and Crohn's colitis. This up-regulation is a response directed to the special types of bacteria recently detected in these diseases. The aim of lysozyme up-regulation is to protect individual mucosal segments to chronic inflammation. The molecular mechanisms connected to the crosstalk between the intraluminal bacterial flora and the production of lysozyme released by the GI mucosae, are discussed. Bacterial resistance continues to exhaust our supply of commercial antibiotics. The potential use of lysozyme to treat infectious diseases is receiving much attention.
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PMID:The Natural Antimicrobial Enzyme Lysozyme is Up-Regulated in Gastrointestinal Inflammatory Conditions. 2543 8

The mucosa of the esophagus, the stomach, the small intestine, the large intestine and rectum are unremittingly challenged by adverse micro-environmental factors, such as ingested pathogenic and non-pathogenic bacteria, and harsh secretions with digestive properties with disparate pH, as well as bacteria and secretions from upstream GI organs. Despite the apparently inauspicious mixture of secretions and bacteria, the normal GI mucosa retains a healthy state of cell renewal. To by-pass the tough microenvironment, the epithelia of the GI react by speeding-up cell exfoliation, by increasing peristalsis, eliminating bacteria through secretion of plasma cell-immunoglobulins and by increasing production of natural antibacterial enzymes (lysozyme) and host defense peptides (defensin-5). Lysozyme was recently found up-regulated in Barrett's esophagitis, in chronic gastritis, in gluten-induced atrophic duodenitis (celiac disease), in collagenous colitis, in lymphocytic colitis and in Crohn's colitis. This up-regulation is a response directed towards the special types of bacteria thriving in the microenvironment in each of the aforementioned clinical inflammatory maladies. The purpose of that up-regulation is to protect the mucosa affected by the ongoing chronic inflammation. Bacterial antibiotic resistance continues to exhaust our supply of effective antibiotics. The future challenge is how to solve the increasing menace of bacterial resistance to anti-bacterial drugs. Further research on natural anti-bacterial enzymes such as lysozyme, appears mandatory.
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PMID:Increased Production of Lysozyme Associated with Bacterial Proliferation in Barrett's Esophagitis, Chronic Gastritis, Gluten-induced Atrophic Duodenitis (Celiac Disease), Lymphocytic Colitis, Collagenous Colitis, Ulcerative Colitis and Crohn's Colitis. 2663 45