Alterations in polyamine metabolism induced by the pathogen Helicobacter pylori: Implications for gastric
Alain P Gobert1, Caroline V Hawkins2, Kara M McNamara3
1Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States; Center for Mucosal Inflammation and Cancer, Vanderbilt University Medical Center, Nashville, TN, United States; Program in Cancer Biology, Vanderbilt University Medical Center, Nashville, TN, United States.
Abstract:
Helicobacter pylori is a pathogen of the human stomach that infects half of the world's population. The chronicity of the infection is a major risk factor for the development of gastric cancer. Multiple parameters, including the heterogenicity of the virulence factors, the environmental parameters, or the intensity of the host responses, regulate the evolution of the disease. Thus, we have reported that the dysregulation of the polyamine pathway in the infected gastric mucosa represents a major component of the inflammation and the risk for neoplastic transformation. Using different animal models and gastric organoids, we recently highlighted the critical role of spermine oxidase-derived acrolein in the pathogenesis of H. pylori infection and the progression to carcinoma. Herein, we describe the experimental procedures that have been used, from the culture of the bacteria to the various models of infection in vivo and in vitro, and the assessment of acrolein generation.
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