Abstract
Helicobacter pylori, a gastroenteric pathogen believed to have co-evolved with humans over 100,000 years, shows significant genetic variability. This motivates the study of different H. pylori strains and the diseases they cause in order to identify determinants for disease evolution. In this study, we used proteomics tools to compare two H. pylori strains. Nic25_A was isolated in Nicaragua from a patient with intestinal metaplasia, and P12 was isolated in Europe from a patient with duodenal ulcers. Differences in the abundance of surface proteins between the two strains were determined with two mass spectrometry-based methods, label-free quantification (MaxQuant) or the use of tandem mass tags (TMT). Each approach used a lipid-based protein immobilization (LPITM) technique to enrich peptides of surface proteins. Using the MaxQuant software, we found 52 proteins that differed significantly in abundance between the two strains (up- or downregulated by a factor of 1.5); with TMT, we found 18 proteins that differed in abundance between the strains. Strain P12 had a higher abundance of proteins encoded by the cag pathogenicity island, while levels of the acid response regulator ArsR and its regulatory targets (KatA, AmiE, and proteins involved in urease production) were higher in strain Nic25_A. Our results show that differences in protein abundance between H. pylori strains can be detected with proteomic approaches; this could have important implications for the study of disease progression.
Highlights
Helicobacter pylori is a Gram-negative, spiral shaped ε-proteobacterium that colonizes the stomachs of roughly half the world’s population (Brown, 2000)
Our aim was to evaluate and compare genetic content and protein abundance between two pathogenic strains of H. pylori; strain P12 was isolated in Europe from a patient with duodenal ulcers, and strain Nic25_A was isolated in Nicaragua from the antrum of a patient with atrophy and intestinal metaplasia
Several single nucleotide variants (SNVs) between the two H. pylori strains were distributed along the chromosome and accounted for about 1.1% of the total nucleotides in the H. pylori P12 chromosome (Supporting Files 1–3)
Summary
Helicobacter pylori is a Gram-negative, spiral shaped ε-proteobacterium that colonizes the stomachs of roughly half the world’s population (Brown, 2000). Infection with H. pylori typically causes a mild, mixed gastritis; chronic infections cause severe clinical outcomes, such as duodenal and gastric ulcers, in approximately 15% of infected individuals. The coexistence of gastric cancer and duodenal ulcer in the same individual is Genomics and Mass Spectrometry-Based Proteomics in H. Chronic H. pylori infection contributes to gastric issues that are associated with the development of gastric cancer, such as the loss of acid secretion and the loss of acidic mammalian chitinase expression (Nookaew et al, 2013). The factors leading to this divergence in clinical outcomes are not entirely known, but host genetics that regulate the potency of the immune response toward the infection, bacterial genetics, and environmental factors, such as diet and smoking, contribute (Ahn and Lee, 2015)
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