Abstract
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.
Highlights
After birth, the cells that line the mucosa of the human gastrointestinal (GI) tract are increasingly threatened by adverse micro-environmental conditions, such as digestive juices of different pH, a wide variety of active enzymes, and enormous amounts of bacteria
In a series of immuno-histochemical studies lysozyme was found up-regulated in many organs of the GI undergoing chronic inflammation, such as Barrett’s oesophagitis, chronic gastritis, gluten-induced atrophic duodenitis, collagenous colitis, lymphocytic colitis, ulcerative colitis (UC), and Crohn’s colitis [7,8,9,10], strongly suggesting that the associated bacterial flora plays an important role in the expression of this antimicrobial enzyme
Our studies [8,49] suggest that that gastric intestinal metaplasia and gastric atrophy are two different biological processes, atrophy being the result of the local destruction of glands by the chronic inflammation, and intestinal metaplasia, the consequence of an adaptive enzymatic up-regulation aimed to protect the mucosa from proliferating bacteria
Summary
The cells that line the mucosa of the human gastrointestinal (GI) tract are increasingly threatened by adverse micro-environmental conditions, such as digestive juices of different pH, a wide variety of active enzymes, and enormous amounts of bacteria. Cocktails of bacteria and secretions from upper organs challenge the epithelia of downstream organs along the tract
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