Generation of Ammonia and Mucosal Lesion Formation Following Hydrolysis of Urea by Urease in the Rat Stomach

Helicobacter pylori: A Brief History of a Still Lacking Vaccine

“…H. pylori urease consists of two moieties, UreA (27 kDa) and UreB (62 kDa), and constitutes up to 10% of the total bacterial protein content. The production of ammonia is able to produce histological damage in the gastric mucosa [58]. Moreover, urease may contribute to mucosal damage through local activation of inflammatory cells [59,60],…”

Tripping on Acid: Trans-Kingdom Perspectives on Biological Acids in Immunity and Pathogenesis

“…A significant human pathogen that provides an understanding of an alternative strategy by which an extracellular acidic niche can be occupied is Helicobacter pylori , the agent whose colonization is associated with chronic gastrointestinal diseases ranging from dyspepsia to gastric and duodenal ulcers to gastric carcinoma [101], [102]. This organism chronically infects the stomach, surviving the very low pH of the lumen, burrowing into the mucus with flagella to attach to and occasionally invade epithelial cells.…”

“…This organism chronically infects the stomach, surviving the very low pH of the lumen, burrowing into the mucus with flagella to attach to and occasionally invade epithelial cells. Survival in this environment is dependent on expression of copious amounts of urease, converting urea into buffering ammonia plus carbon dioxide [102]. In this strategy, H. pylori maintains a periplasmic pH at ∼6.1, while the extracellular environment can be as low as 2.0.…”

Helicobacter pyloriand Microcirculation

“…On the other hand, Hp urease‐dependent ammonia production is inevitable for the existence of Hp in an acidic environment. This ammonia also exerts toxic effects on the gastric mucosa [ 37 ]. Warzecha et al [ 61 ] demonstrated that histamine and gastric acid secretion exhibit a protective effect against ammonia‐induced gastric damage, possibly through stimulation of gastrin secretion and PGE 2 production, and improvement of the gastric mucosal microcirculation.…”

“…The initial search terms yielded 69 original English‐language manuscripts. Among these, 45 dealt with the pathophysiological and clinical aspects of Hp infection focusing on the microcirculation, including 25 describing animal studies [ 22 , 25 , 6 , 27 , 7 , 31 , 54 , 21 , 13 , 24 , 10 , 64 , 45 , 3 , 29 , 9 , 8 , 32 , 46 , 67 , 28 , 61 , 62 , 55 , 37 ], four describing studies on human cells [ 25 , 60 , 26 , 30 ], and 16 describing human studies [ 16 , 65 , 1 , 2 , 59 , 34 , 48 , 35 , 42 , 19 , 38 , 39 , 66 , 33 , 15 , 11 ]. Then, the extracted pathophysiological and clinical aspects of Hp and microcirculation were reported descriptively.…”