Increased Gastric Osteopontin Expression by Helicobacter pylori Infection can Correlate with More Severe Gastric Inflammation and Intestinal Metaplasia

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Abstract

Background: Osteopontin (OPN) is involved in the gastric cancer progression. The study validated whether OPN expressions correlate with Helicobacter pylori-related chronic gastric inflammation and the precancerous change as intestinal metaplasia (IM). Methods: This study included 105 H. pylori-infected patients (63 without and 42 with IM) and 29 H. pylori-negative controls. In each subject, the gastric OPN expression intensity was evaluated by immunohistochemistry, and graded from 0 to 4 for the epithelium, lamina propria, and areas with IM, respectively. For the H. pylori-infected subjects, the gastric inflammation was assessed by the Updated Sydney System. Forty-nine patients received follow-up endoscopy to assess OPN change on gastric mucosa after H. pylori eradication. The in vitro cell-H. pylori coculture were performed to test the cell origin of OPN. Results: The H. pylori-infected patients had higher gastric OPN expression than the noninfected controls (p<001). For the H. pylori-infected patients, an increased OPN expression correlated with more severe chronic gastric inflammation (p<001) and the presence of IM (OR: 2.6, 95% CI: 1.15-5.94, p=02). Within the same gastric bits, lamina propria expressed OPN stronger than epithelium (p<001), suggesting OPN predominantly originates from inflammatory cells. The in vitro assay confirmed H. pylori stimulate OPN expression in the monocytes, but not in the gastric epithelial cells. After H. pylori eradication, the gastric OPN expression could be decreased only in areas without IM (p<05). Conclusions: Increased gastric OPN expression by H. pylori infection can correlate with a more severe gastric inflammation and the presence of IM.

Original languageEnglish
Pages (from-to)217-224
Number of pages8
JournalHelicobacter
Volume16
Issue number3
DOIs
Publication statusPublished - 2011 Jun 1

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Osteopontin
Metaplasia
Helicobacter Infections
Helicobacter pylori
Stomach
Inflammation
Mucous Membrane
Epithelium
Coculture Techniques
Gastric Mucosa
Endoscopy
Stomach Neoplasms
Monocytes
Epithelial Cells
Immunohistochemistry

All Science Journal Classification (ASJC) codes

  • Gastroenterology
  • Infectious Diseases

Cite this

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title = "Increased Gastric Osteopontin Expression by Helicobacter pylori Infection can Correlate with More Severe Gastric Inflammation and Intestinal Metaplasia",
abstract = "Background: Osteopontin (OPN) is involved in the gastric cancer progression. The study validated whether OPN expressions correlate with Helicobacter pylori-related chronic gastric inflammation and the precancerous change as intestinal metaplasia (IM). Methods: This study included 105 H. pylori-infected patients (63 without and 42 with IM) and 29 H. pylori-negative controls. In each subject, the gastric OPN expression intensity was evaluated by immunohistochemistry, and graded from 0 to 4 for the epithelium, lamina propria, and areas with IM, respectively. For the H. pylori-infected subjects, the gastric inflammation was assessed by the Updated Sydney System. Forty-nine patients received follow-up endoscopy to assess OPN change on gastric mucosa after H. pylori eradication. The in vitro cell-H. pylori coculture were performed to test the cell origin of OPN. Results: The H. pylori-infected patients had higher gastric OPN expression than the noninfected controls (p<001). For the H. pylori-infected patients, an increased OPN expression correlated with more severe chronic gastric inflammation (p<001) and the presence of IM (OR: 2.6, 95{\%} CI: 1.15-5.94, p=02). Within the same gastric bits, lamina propria expressed OPN stronger than epithelium (p<001), suggesting OPN predominantly originates from inflammatory cells. The in vitro assay confirmed H. pylori stimulate OPN expression in the monocytes, but not in the gastric epithelial cells. After H. pylori eradication, the gastric OPN expression could be decreased only in areas without IM (p<05). Conclusions: Increased gastric OPN expression by H. pylori infection can correlate with a more severe gastric inflammation and the presence of IM.",
author = "Wei-Lun Chang and Yang, {Hsiao Bai} and Hsiu-Chi Cheng and Chiao-Hsiung Chuang and Pei-Jung Lu and Bor-Shyang Sheu",
year = "2011",
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T1 - Increased Gastric Osteopontin Expression by Helicobacter pylori Infection can Correlate with More Severe Gastric Inflammation and Intestinal Metaplasia

AU - Chang, Wei-Lun

AU - Yang, Hsiao Bai

AU - Cheng, Hsiu-Chi

AU - Chuang, Chiao-Hsiung

AU - Lu, Pei-Jung

AU - Sheu, Bor-Shyang

PY - 2011/6/1

Y1 - 2011/6/1

N2 - Background: Osteopontin (OPN) is involved in the gastric cancer progression. The study validated whether OPN expressions correlate with Helicobacter pylori-related chronic gastric inflammation and the precancerous change as intestinal metaplasia (IM). Methods: This study included 105 H. pylori-infected patients (63 without and 42 with IM) and 29 H. pylori-negative controls. In each subject, the gastric OPN expression intensity was evaluated by immunohistochemistry, and graded from 0 to 4 for the epithelium, lamina propria, and areas with IM, respectively. For the H. pylori-infected subjects, the gastric inflammation was assessed by the Updated Sydney System. Forty-nine patients received follow-up endoscopy to assess OPN change on gastric mucosa after H. pylori eradication. The in vitro cell-H. pylori coculture were performed to test the cell origin of OPN. Results: The H. pylori-infected patients had higher gastric OPN expression than the noninfected controls (p<001). For the H. pylori-infected patients, an increased OPN expression correlated with more severe chronic gastric inflammation (p<001) and the presence of IM (OR: 2.6, 95% CI: 1.15-5.94, p=02). Within the same gastric bits, lamina propria expressed OPN stronger than epithelium (p<001), suggesting OPN predominantly originates from inflammatory cells. The in vitro assay confirmed H. pylori stimulate OPN expression in the monocytes, but not in the gastric epithelial cells. After H. pylori eradication, the gastric OPN expression could be decreased only in areas without IM (p<05). Conclusions: Increased gastric OPN expression by H. pylori infection can correlate with a more severe gastric inflammation and the presence of IM.

AB - Background: Osteopontin (OPN) is involved in the gastric cancer progression. The study validated whether OPN expressions correlate with Helicobacter pylori-related chronic gastric inflammation and the precancerous change as intestinal metaplasia (IM). Methods: This study included 105 H. pylori-infected patients (63 without and 42 with IM) and 29 H. pylori-negative controls. In each subject, the gastric OPN expression intensity was evaluated by immunohistochemistry, and graded from 0 to 4 for the epithelium, lamina propria, and areas with IM, respectively. For the H. pylori-infected subjects, the gastric inflammation was assessed by the Updated Sydney System. Forty-nine patients received follow-up endoscopy to assess OPN change on gastric mucosa after H. pylori eradication. The in vitro cell-H. pylori coculture were performed to test the cell origin of OPN. Results: The H. pylori-infected patients had higher gastric OPN expression than the noninfected controls (p<001). For the H. pylori-infected patients, an increased OPN expression correlated with more severe chronic gastric inflammation (p<001) and the presence of IM (OR: 2.6, 95% CI: 1.15-5.94, p=02). Within the same gastric bits, lamina propria expressed OPN stronger than epithelium (p<001), suggesting OPN predominantly originates from inflammatory cells. The in vitro assay confirmed H. pylori stimulate OPN expression in the monocytes, but not in the gastric epithelial cells. After H. pylori eradication, the gastric OPN expression could be decreased only in areas without IM (p<05). Conclusions: Increased gastric OPN expression by H. pylori infection can correlate with a more severe gastric inflammation and the presence of IM.

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