Helicobacter pylori infection: Physiopathologic implication of Nα-methyl histamine

Putative effect ofHelicobacter pyloriand gastritis on gastric acid secretion in cat

“…Further evidence for this is provided by the increase in acid secretion induced by thioperamide before eradication therapy, resulting in levels of acid secretion similar to those recorded after eradication. These findings are consistent with previous data obtained in vitro and in vivo by ourselves (3,11) and others (7,16,42,43,52).…”

“…We cannot exclude the possibility that a similar mechanism operates in the model studied here. Alternatively, the inhibition of gastric acid secretion may be accounted for by changes in histidine decarboxylase (HDC) activity (11,16,42,43). H. pylori infection is indeed usually associated with a decrease in the histamine content in the mucosa, probably due to the downregulation of HDC activity.…”

“…H. pylori infection is indeed usually associated with a decrease in the histamine content in the mucosa, probably due to the downregulation of HDC activity. This may be brought about by the action of N␣-MH on H 3 receptors (7,11). Histamine, released from ECL or mast cells, stimulates acid secretion via H 2 receptors on parietal cells.…”

“…Not only does H. pylori have urease activity, enabling it to neutralize acid by an ammonia buffer system, it also produces an inhibitory toxin that binds H ϩ -K ϩ -ATPase (15). In addition, it produces N␣-methylhistamine (N␣-MH), a potent H 3 receptor agonist (1,3,5,11). Indeed, H 3 receptor agonists may inhibit gastric secretion by exerting an inhibitory effect on enterochromaffin-like (ECL) cells (41).…”

Histamine 3 receptor activation mediates inhibition of acid secretion duringHelicobacter-induced gastritis

“…Cou rillonMallet et al first revealed elevated concentrations of H3R agonist Nαmethylhistamine (NαMH) in the gastric mucosa of H. pylori infected patients [1,5,6] . NαMH has an indirect inhibitory effect on acid secretion by inhibiting the acid secretagogue histamine from the ECLlike ce lls [3,5] . Stimulation of H3Rs on ECLlike cells eventually inhibits histidine decarboxylase (HDC) activity [3,5] .…”