Helicobacter pylori promotes hepatic fibrosis in the animal model

Moon Jung Goo, Mi Ran Ki, Hye Rim Lee, Hai Jie Yang, Dong Wei Yuan, Il Hwa Hong, Jin Kyu Park, Kyung Sook Hong, Jung Youn Han, Ok Kyung Hwang, Dong Hwan Kim, Sun Hee Do, Ronald D. Cohn, Kyu Shik Jeong

Research output: Contribution to journalArticle

Abstract

Helicobacter pylori infection has been reported to be very common in patients with chronic liver diseases, including cirrhosis. To elucidate the pathological effect of H. pylori infection on the progression of hepatic fibrosis, C57BL/6 mice and Sprague-Dawley rats were orally inoculated with H. pylori, and hepatic fibrosis was induced with carbon tetrachloride (CCl 4) administration. We observed the histopathological changes and the presence of H. pylori genes by PCR in the liver. Significant increase in the fibrotic score as well as in serum alanine aminotransferase and aspartate aminotransferase levels was shown in the CCl 4 H. pylori group compared with that in the CCl 4-treated group. Compared with the CCl 4-treated group, α-smooth muscle actin and transforming growth factor-Β1 were enhanced; however, senescence marker protein-30, a multifunctional protein protecting hepatocytes against oxidative stress and apoptosis, was suppressed in the CCl 4 H. pylori group. The 16S rRNA (400 bp) was demonstrated by PCR for H. pylori genes from genomic DNA extracted from the liver, and H. pylori-infected mice showed 93.8% (15 of 16) seropositivity by contrast with seronegativity in all H. pylori-noninfected mice. In addition, immunohistochemical study against H. pylori showed positive antigen fragments in the liver of the infected groups. Consequently, our data suggest that H. pylori infection could be an important contributing infectious factor to the development of liver cirrhosis.

Original languageEnglish (US)
Pages (from-to)1291-1303
Number of pages13
JournalLaboratory Investigation
Volume89
Issue number11
DOIs
StatePublished - Nov 2009

Fingerprint

Helicobacter pylori
Fibrosis
Animal Models
Liver
Helicobacter Infections
Polymerase Chain Reaction
Carbon Tetrachloride
Transforming Growth Factors
Aspartate Aminotransferases
Alanine Transaminase
Inbred C57BL Mouse
Liver Cirrhosis
Genes
Smooth Muscle
Sprague Dawley Rats
Liver Diseases
Actins
Hepatocytes
Proteins
Oxidative Stress

Keywords

  • 16S rRNA
  • Helicobacter pylori
  • Hepatic fibrosis
  • Liver
  • Senescence marker protein 30

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Cell Biology
  • Molecular Biology

Cite this

Goo, M. J., Ki, M. R., Lee, H. R., Yang, H. J., Yuan, D. W., Hong, I. H., ... Jeong, K. S. (2009). Helicobacter pylori promotes hepatic fibrosis in the animal model. Laboratory Investigation, 89(11), 1291-1303. https://doi.org/10.1038/labinvest.2009.90

Helicobacter pylori promotes hepatic fibrosis in the animal model. / Goo, Moon Jung; Ki, Mi Ran; Lee, Hye Rim; Yang, Hai Jie; Yuan, Dong Wei; Hong, Il Hwa; Park, Jin Kyu; Hong, Kyung Sook; Han, Jung Youn; Hwang, Ok Kyung; Kim, Dong Hwan; Do, Sun Hee; Cohn, Ronald D.; Jeong, Kyu Shik.

In: Laboratory Investigation, Vol. 89, No. 11, 11.2009, p. 1291-1303.

Research output: Contribution to journalArticle

Goo, MJ, Ki, MR, Lee, HR, Yang, HJ, Yuan, DW, Hong, IH, Park, JK, Hong, KS, Han, JY, Hwang, OK, Kim, DH, Do, SH, Cohn, RD & Jeong, KS 2009, 'Helicobacter pylori promotes hepatic fibrosis in the animal model', Laboratory Investigation, vol. 89, no. 11, pp. 1291-1303. https://doi.org/10.1038/labinvest.2009.90
Goo MJ, Ki MR, Lee HR, Yang HJ, Yuan DW, Hong IH et al. Helicobacter pylori promotes hepatic fibrosis in the animal model. Laboratory Investigation. 2009 Nov;89(11):1291-1303. https://doi.org/10.1038/labinvest.2009.90
Goo, Moon Jung ; Ki, Mi Ran ; Lee, Hye Rim ; Yang, Hai Jie ; Yuan, Dong Wei ; Hong, Il Hwa ; Park, Jin Kyu ; Hong, Kyung Sook ; Han, Jung Youn ; Hwang, Ok Kyung ; Kim, Dong Hwan ; Do, Sun Hee ; Cohn, Ronald D. ; Jeong, Kyu Shik. / Helicobacter pylori promotes hepatic fibrosis in the animal model. In: Laboratory Investigation. 2009 ; Vol. 89, No. 11. pp. 1291-1303.
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