muramidase and Barrett-Esophagus

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.

Topics: Barrett Esophagus; Celiac Disease; Colitis, Collagenous; Colitis, Lymphocytic; Colitis, Ulcerative; Crohn Disease; Gastritis; Gastrointestinal Diseases; Humans; Inflammation; Muramidase

Lysozyme is a natural antimicrobial enzyme that is up-regulated in inflammatory diseases of the gastrointestinal tract. Pathogenic microbes have recently been identified in the esophageal mucosa in patients with Barrett's esophagus (BE). Lysozyme expression was evaluated in biopsies from patients with BE.. Ninety-seven consecutive esophageal biopsies with columnar-lined Barrett's mucosa (BM) were investigated: 16 had oxyntic gland-only BM, 19 pyloric gland-only BM and 62, intestinal metaplasia BM. Twenty normal gastric biopsies and 20 normal duodenal biopsies were included as controls. Sections were stained with human lysozyme antiserum.. Lysozyme was up-regulated in the neck glands in 94% of the biopsies with oxyntic gland-only BM, in the pyloric gland in 79% of the biopsies with pyloric gland-only BM, and in goblet cells in 65% of the biopsies with intestinal metaplasia BM. Goblet cells with faint lysozyme expression were often found in glands overexpressing lysozyme in mucous secretions in the lumen. When compared to controls, lysozyme was up-regulated in all three BM phenotypes (p<0.05).. Lysozyme is up-regulated in BM. It is therefore, believed that lysozyme's up-regulation might mirror a molecular mechanism of self-defence aimed to safeguard the BM against the hostile pathogenic microbiota present in the esophageal microenvironment in patients with BE.

Topics: Bacteria; Barrett Esophagus; Biopsy; Gene Expression Regulation, Enzymologic; Humans; Immunohistochemistry; Muramidase; Up-Regulation

Topics: Barrett Esophagus; Esophagus; Humans; Mucous Membrane; Muramidase; Up-Regulation

The submucosal glands (SMGs) of the pig esophagus, like the human, secrete mucin and bicarbonate, which help in luminal acid clearance and epithelial protection. The aim of this study was to characterize histochemically the esophageal SMGs and a primary culture obtained from these glands. Tissues and cultures were stained with hematoxylin and eosin, periodic acid Schiff, Alcian blue, lectins, or cytokeratins. In the perfused esophagus, addition of carbachol increased mucin secretion by approximately 2-fold. The results indicate that [1] a method for culturing SMG cells was developed; [2] conventional staining indicates the presence of sulfated, acidic, and neutral mucopolysaccharides in glands and cultures; [3] lectin binding indicates the presence of N-acetyl glucosamine, N-acetyl neuraminic acid, N-acetyl galactosamine, and alpha-L: -fucose in mucous cells and cultures; [4] cytokeratin and lectin staining indicated similarities with Barrett epithelium (columnar metaplasia of the esophagus); and [5] cholinergic agonists enhance mucin secretion and this could play a significant role in esophageal protection.

Topics: Animals; Barrett Esophagus; Bicarbonates; Biomarkers; Cells, Cultured; Cholinergic Agonists; Esophagus; Fluorescent Antibody Technique; Immunoenzyme Techniques; Intestinal Mucosa; Keratins; Lectins; Mucins; Muramidase; Swine