Gastroduodenal mucosal defense

Abstract

Purpose of review-To review recent developments in the field of gastroduodenal mucosal defense.Recent findings-Research in the field of gastroduodenal mucosal defense has focused on continued elucidation of molecular mechanisms that protect the mucosa and influence healing at the cellular level. Review of literature over the past year reveals that familiar proteins and mediators such as nitric oxide, Toll-like receptors, nucleotide-binding oligomerization domaincontaining proteins, β-defensins, macrophages, dendritic cells, mucins, autophagy, and the influence of aging and diet are still subjects of study, but also brings into light new processes and mediators such as dual oxidases, defense against radiation injuries, and novel proteins such as ZBP-89.Summary-These new published findings contribute to our overall understanding of gastroduodenal defense and suggest innovative avenues of future research and possible novel therapeutic targets.

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

“…Urease, in addition to its role in acid neutralization, contributes to H.p. pathogenicity by production ammonia (disrupts cell junctions and damages epithelium) and reactive oxygen species (ROS), activating lipoxygenase, inducing angiogenesis, hypoxia-induced factor and apoptosis [ 26 , 27 , 28 , 29 , 30 ]. The helical shape and flagella, two factors responsible for bacterial mobility, also contribute to colonization and persistence of the infection (allow H.p.…”

Dietary Nitrate and the Epidemiology of Cardiovascular Disease: Report From a National Heart, Lung, and Blood Institute Workshop

“…The resulting microbial-produced nitrite is swallowed, whereupon much of it is absorbed through the gastrointestinal tract as nitrite and some of it is reduced to nitric oxide in the stomach; the nitric oxide so produced contributes to gastric mucosa integrity and provides protection against colonization of the stomach by infectious agents. [6][7][8] Plasma nitrate levels rise immediately after a nitrate-rich meal, with a half-life of %5 hours, and plasma nitrite levels subsequently rise in parallel, slightly delayed by the enterosalivary cycling for the reduction of nitrate to nitrite. 9,10 Practitioners of ancient Chinese medical arts demonstrated empirical knowledge of this enterosalivary cycle: These healers wrote that while administering saltpeter (potassium nitrate) for heart pain, it is important for the patient to swallow any saliva that is produced.…”

Muc5ac null mice are predisposed to spontaneous gastric antro-pyloric hyperplasia and adenomas coupled with attenuated H.pylori-induced corpus mucous metaplasia

“…A complex interplay exists between Hp and the host's gastric mucosa leading to persistent Hp colonization within the stomach often for a lifetime (1,2). The gastric lumen-surface epithelial interface is characterized by its' acidic pH, lack of nutrients, high viscosity mucus, continuous clearance of luminal contents by peristaltic action, epithelial cell turnover, infiltrating inflammatory cells and the host's innate and adaptive immune responses (3,4,5). Upon gastric infection, Hp encounters the protective mucous layer which is composed primarily of mucins and many other glycoproteins (3,4,5).…”