Epithelium gastric

Helicobacter pylori normally resides in the human stomach and is transmitted via the fecal-oral route or through ingestion of fecal-contaminated water or food. Infection with HP is more common in developing countries because of crowded conditions and the presence of contaminated food and water. HP colonization does not necessarily reflect an active infection since the organism can attach itself to the gastric epithelium... 

Nonselective NSAIDs (including aspirin) cause gastric mucosal damage by two mechanisms (1) a direct or topical irritation of the gastric epithelium, and (2) systemic inhibition of the cyclooxygenase-1 (COX-1) enzyme, which results in decreased synthesis of protective prostaglandins. 

Helicobacter pylori to human gastric epithelium.26 Clinical studies have identified H. pylori as a causative agent in gastric and duodenal ulcers.27 Considerable evidence exists to suggest that carbohydrate-based treatments could be an effective means to combat infection.28 Since bacterial attachment is a prerequisite to infection,29 soluble Leb oligosaccharides may serve as therapeutic alternatives to broad-spectrum antibiotics. 

Mahdavi, J., Boren, T., Vandenbroucke-Graula, C., and AppehneUc, B. J. (2003). Limited role of lipopolysaccharide Lewis antigens in adherence of Helicobacter pylori to the human gastric epithelium. Infect. Immun. 71, 2876-2880. 

Representing >20% of bile, are strong sulphonic acids with detergent properties. They are soluble in the normal acidic stomach, with pKa values of <2. Thus they can partially enter the gastric epithelium. It is also known that epithelial diffusion barriers can be broken by BAs, which further allow them entry into the epithelium. 

Interaction with local tissues. Sucralfate appears to augment the protective function of the mucous-bicarbonate barrier, partly due to increased bicarbonate and mucous secretion, and partly to an interaction with the unstirred layer overlying gastric epithelium, as well as by making the mucous gel more hydrophobic. It binds bile acids and pepsin and adheres to both ulcerated and nonulcerated mucosa. 

Strassburg CP, Nguyen N, Manns MP, et al. Polymorphic expression of the UDP-glucuronosyltransferase UGT1A gene locus in human gastric epithelium. Mol Pharmacol 1998 54(4) 647-654. 

Matsumoto Y, Marusawa H, Kinoshita K et al (2007) Helicobacter pylori infection triggers aberrant expression of activation-induced cyti-dine deaminase in gastric epithelium. Nat Med 13 470—476... 

Parallel Operation of K+/H+ exchange and (X/HCO3 cotransport Amphiuma red cells, frog skin, cornea K+/H+ ATPase gastric epithelium... 

Null Occludin Growth retardation, male sterility, chronic inflammation, hyperplasia of gastric epithelium, brain calcification... 

Schmausser, B., AndruUs, M., Endrich, S., Lee, S.K., Josenhans, C., Muller-Hermelink, H.K., Eck, M. Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection. Clin Exp Immunol 136 (2004) 521-526. 

There is very limited evidence for CYP expression in the human stomach. Furthermore, it is difficult to propose any function for gastric CYPs because the gastric epithelium secretes rather than absorbs. However, the potential of those CYPs expressed in the stomach to play roles in stomach cancer has been investigated in cases of intestinal metaplasia of the stomach. Intestinal metaplasia of the stomach, which involves the replacement of the gastric mucosa with a small intestine-like epithelium (100), is considered to be a precancerous lesion (101). A combination... 

Peptic ulcer disease is associated with Helicobacter pylori infection in 90% of patients with gastric and duodenal ulceration. Elimination of H. pylori infection with antibiotics heals the peptic ulcer and the associated symptoms. Combination therapy with antibiotics, anti-secretory agents, namely H2-receptor antagonists or proton pump inhibitors, and bismuth salts has significantly improved the clinical outcome of peptic ulcer disease. Not all strains of H. pylori cause peptic ulcer disease, and other factors are necessary for H. pylori colonization and disease to occur. Flagellated motile bacteria resist peristalsis and adhere to gastric epithelium in a highly specific manner. 

Abstract Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for the development of peptic ulcer disease and gastric cancer. Adhesion of microbes to the target tissue is an important determinant for successful initiation, establishment and maintenance of infection, and a variety of different candidate carbohydrate receptors for H. pylori have been identified. Here the different the binding specifities, and their potential role in adhesion to human gastric epithelium are described. Finally, recent findings on the roles of sialic acid binding SabA adhesin in interactions with human neutrophils and erythrocytes are discussed. 

H. pylori has a very narrow host and tissue range and has only been found in connection with gastric epithelium from humans and monkeys [48], In the H. pylori-infected stomach the majority of the bacteria are found within the gastric mucus layer, while approximately 20% of the H. pylori population are found attached to the gastric epithelial cells. 

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