pylori [123]. During an ongoing infection of Helicobacter pylori, macrophages display an increase level of SMO, which results in mitochondrial mediated apoptosis and the release of hydrogen peroxide into the extracellular space causing the damage of adjacent epithelial cells in the stomach [124] Recent publications argue that Helicobacter pylori causes an increase in the amount inducible NO synthase (iNOS) and NO [125]. At the same time arginase II is induced which results in the generation of ornithine and ornithine decarboxylase triggering the generation of polyamines. Spermine, a polyamine impede the proinflammation response; by inhibiting induce NO synthase and NO production [126]. This allows the Helicobacter pylori to sustain and prolong its survival in the stomach [125, 126]
pylori [123]. During an ongoing infection of Helicobacter pylori, macrophages display an increase level of SMO, which results in mitochondrial mediated apoptosis and the release of hydrogen peroxide into the extracellular space causing the damage of adjacent epithelial cells in the stomach [124] Recent publications argue that Helicobacter pylori causes an increase in the amount inducible NO synthase (iNOS) and NO [125]. At the same time arginase II is induced which results in the generation of ornithine and ornithine decarboxylase triggering the generation of polyamines. Spermine, a polyamine impede the proinflammation response; by inhibiting induce NO synthase and NO production [126]. This allows the Helicobacter pylori to sustain and prolong its survival in the stomach [125, 126]