Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages

Dah Yuu Lu, Chin Hsin Tang, Chia Hsian Chang, Ming Chei Maa, Shih Hua Fang, Yuan Man Hsu, Yu Hsin Lin, Chun Jung Lin, Wan Chi Lee, Hwai Jeng Lin, Che Hsin Lee, Chih Ho Lai

研究成果: 雜誌貢獻文章

15 引文 (Scopus)

摘要

Intragastric growth of Helicobacter pylori and non-Helicobacter microorganisms is thought to be associated with elevated levels of pro-inflammatory cytokines and the production of NO these effects can lead to chronic inflammation. Microorganisms can activate the expression of iNOS and the production of NO by macrophages through stimulation with bacterial LPS. Helicobacter pylori can evade these vigorous immune responses, but the underlying mechanism remains unknown. In this study, we used a murine model of macrophage infection to demonstrate that H. pylori inhibits LPS-induced expression of iNOS and production of NO by macrophages. Suppression of LPS-induced NO production by macrophages led to elevated survival of H. pylori in a trans-well system. This effect was abrogated in macrophages from iNOS-/- mice. Analysis of iNOS mRNA and protein levels revealed that H. pylori inhibits iNOS expression at both transcriptional and post-transcriptional levels, and that these effects occurred with live bacteria. Furthermore, the effect of H. pylori involved down-regulation of the mitogen-activated protein kinase pathway and the translocation of active NF-κB into the nucleus. Taken together, our results reveal a new mechanism by which H. pylori modulates the innate immune responses of the host and maintains a persistent infection within the stomach.

原文英語
頁(從 - 到)406-417
頁數12
期刊Innate Immunity
18
發行號3
DOIs
出版狀態已發佈 - 六月 2012

指紋

Helicobacter pylori
Nitric Oxide
Macrophages
Infection
Mitogen-Activated Protein Kinases
Innate Immunity
Helicobacter pylori lipopolysaccharide
Stomach
Down-Regulation
Cytokines
Inflammation
Bacteria
Messenger RNA
Growth
Proteins

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Immunology
  • Microbiology
  • Infectious Diseases

引用此文

Lu, D. Y., Tang, C. H., Chang, C. H., Maa, M. C., Fang, S. H., Hsu, Y. M., ... Lai, C. H. (2012). Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages. Innate Immunity, 18(3), 406-417. https://doi.org/10.1177/1753425911413164

Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages. / Lu, Dah Yuu; Tang, Chin Hsin; Chang, Chia Hsian; Maa, Ming Chei; Fang, Shih Hua; Hsu, Yuan Man; Lin, Yu Hsin; Lin, Chun Jung; Lee, Wan Chi; Lin, Hwai Jeng; Lee, Che Hsin; Lai, Chih Ho.

於: Innate Immunity, 卷 18, 編號 3, 06.2012, p. 406-417.

研究成果: 雜誌貢獻文章

Lu, DY, Tang, CH, Chang, CH, Maa, MC, Fang, SH, Hsu, YM, Lin, YH, Lin, CJ, Lee, WC, Lin, HJ, Lee, CH & Lai, CH 2012, 'Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages', Innate Immunity, 卷 18, 編號 3, 頁 406-417. https://doi.org/10.1177/1753425911413164
Lu, Dah Yuu ; Tang, Chin Hsin ; Chang, Chia Hsian ; Maa, Ming Chei ; Fang, Shih Hua ; Hsu, Yuan Man ; Lin, Yu Hsin ; Lin, Chun Jung ; Lee, Wan Chi ; Lin, Hwai Jeng ; Lee, Che Hsin ; Lai, Chih Ho. / Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages. 於: Innate Immunity. 2012 ; 卷 18, 編號 3. 頁 406-417.
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