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Proteomic analysis reveals molecular biological details in varioliform gastritis without Helicobacter pylori infection.

ABSTRACT: AIM:To investigate and elucidate the molecular mechanism underlying varioliform gastritis for early detection, prevention and intervention of gastric cancer. METHODS:A combination of two-dimensional gel electrophoresis and mass spectrometry was used to detect the differentially expressed proteins between varioliform gastritis and matched normal mucosa. The selected proteins were confirmed by Western blotting and reverse transcription polymerase chain reaction (RT-PCR) in additional samples and the function of some proteins in varioliform gastritis was analyzed by bio-method preliminarily. RESULTS:We identified 21 differentially expressed proteins in varioliform gastritis, and compared them with matched normal mucosa. Eleven proteins were upregulated and ten downregulated in varioliform gastritis when compared with the same proteins in individual-matched normal gastric mucosa. These proteins are related to metabolism, oxidation, cytoskeleton, apoptosis, signal transduction and other aspects of cells. Two novel proteins, thioredoxin domain-containing protein 5 (TXNDC5) upregulated in varioliform gastritis, and neuropolypeptide h3 [phosphatidylethanolamine-binding protein 1 (PEBP1)] downregulated in varioliform gastritis, were further investigated. Their expressions were validated by Western blotting and RT-PCR in 12 cases of varioliform gastritis which was matched with normal mucosa. The expression level of PEBP1 in varioliform gastritis was significantly lower (P < 0.05) while that of TXNDC5 was significantly higher than that in matched normal gastric mucosa (P < 0.05). CONCLUSION:There are some changes of protein expression in varioliform gastritis. Downregulation of PEBP1 and upregulation of TXNDC5 are involved in the development of varioliform gastritis.

SUBMITTER: Zhang L

PROVIDER: S-EPMC2915426 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature

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Proteomic analysis reveals molecular biological details in varioliform gastritis without Helicobacter pylori infection.

Zhang Lin L Hou Yan-Hong YH Wu Kai K Zhai Jun-Shan JS Lin Nan N

World journal of gastroenterology 20100801 29

<h4>Aim</h4>To investigate and elucidate the molecular mechanism underlying varioliform gastritis for early detection, prevention and intervention of gastric cancer.<h4>Methods</h4>A combination of two-dimensional gel electrophoresis and mass spectrometry was used to detect the differentially expressed proteins between varioliform gastritis and matched normal mucosa. The selected proteins were confirmed by Western blotting and reverse transcription polymerase chain reaction (RT-PCR) in additiona ...[more]

PMID: 20677338

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Project description:ObjectiveThe present study aims to investigate the effect of Helicobacter pylori (Hp) infection on gastric mucosal microbiota in patients with chronic gastritis.MethodsHere recruited a population of 193 patients with both chronic gastritis and positive rapid urease, including 124 patients with chronic atrophic gastritis (CAG) and 69 patients with chronic non-atrophic gastritis (nCAG). Immunoblotting was used to detect four serum Hp antibodies (UreA, UreB, VacA and CagA) to determine the types of virulent Hp-I and avirulent Hp-II infections. Gastric microbiota was profiled by 16S rRNA gene V3-V4 region, and R software was used to present the relationship between the microbial characteristics and the type of Hp infection.ResultsIn the stomach of patients with Hp-positive gastritis, the dominant gastric bacterial genera included Ralstonia (23.94%), Helicobacter (20.28%), Pseudonocardia (9.99%), Mesorhizobium (9.21%), Bradyrhizobium (5.05%), and Labrys (4.75%). The proportion of Hp-I infection was significantly higher in CAG patients (91.1%) than in nCAG patients (71.0%) (P < 0.001). The gastric microbiota richness index (observed OTUs, Chao) was significantly lower in CAG patients than in nCAG patients (P <0.05). Compared with avirulent Hp-II infection, virulent Hp-I infection significantly decreased the Shannon index in CAG patients (P <0.05). In nCAG patients, Hp-I infected patients had lower abundances of several dominant gastric bacteria (Aliidiomarina, Reyranella, Halomonas, Pseudomonas, Acidovorax) than Hp-II infected patients. Meanwhile, in CAG patients, Hp-I infected patients occupied lower abundances of several dominant oral bacteria (Neisseria, Staphylococcus and Haemophilus) than Hp-II infected patients. In addition, bile reflux significantly promoted the colonization of dominant oral microbiota (Veillonella, Prevotella 7 and Rothia) in the stomach of CAG patients. There was no significant symbiotic relationship between Helicobacter bacteria and non-Helicobacter bacteria in the stomach of nCAG patients, while Helicobacter bacteria distinctly linked with the non-Helicobacter bacteria (Pseudolabrys, Ralstonia, Bradyrhizobium, Mesorhizobium and Variovorax) in CAG patients.ConclusionsVirulent Hp infection alters the gastric microbiota, reduces microbial diversity, and enhances the symbiotic relationship between the Helicobacter bacteria and non-Helicobacter bacteria in patients with chronic gastritis. The data provides new evidence for treating Hp infection by improving the gastric microbiota.

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Proteomic analysis reveals molecular biological details in varioliform gastritis without Helicobacter pylori infection.

Publications

Proteomic analysis reveals molecular biological details in varioliform gastritis without Helicobacter pylori infection.

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