Keith Wilson
Faculty Member
Last active: 11/2/2019

Methods to evaluate alterations in polyamine metabolism caused by Helicobacter pylori infection.

Gobert AP, Chaturvedi R, Wilson KT
Methods Mol Biol. 2011 720: 409-25

PMID: 21318889 · PMCID: PMC3069756 · DOI:10.1007/978-1-61779-034-8_26

Helicobacter pylori is a Gram-negative bacteria that infects the human stomach of half of the world's -population. Colonization is followed by infiltration of the gastric mucosa by lymphocytes and myeloid cells. These cells are activated by various bacterial factors, causing them to produce immune/inflammatory mediators, including reactive nitrogen species and polyamines that contribute to cellular damage and the pathogenesis of H. pylori-associated gastric cancer. In vitro experiments have revealed that H. pylori induces macrophage polyamine production by upregulation of the arginase 2/ornithine decarboxylase (ODC) metabolic pathway and enhances hydrogen peroxide synthesis through the activity of spermidine oxidase (SMO). In this chapter, we present a survey of the methods used to analyze the induction and the role of the enzymes related to polyamine metabolism, i.e., arginase, ODC, and SMO in H. pylori-infected macrophages.

MeSH Terms (22)

Acetyltransferases Animals Apoptosis Arginase Arsenicals Biochemistry Cells, Cultured Enzyme Assays Helicobacter Infections Helicobacter pylori Humans Immunoblotting Luciferases Macrophages Mice Nitrogen Dioxide Ornithine Decarboxylase Oxidoreductases Acting on CH-NH Group Donors Polyamines Promoter Regions, Genetic RNA, Messenger Transfection

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