title: Helicobacter pylori promotes hepatic fibrosis in the animal model.
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, alpha-smooth muscle actin and transforming growth factor-beta1 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.
authors.affiliation: Department of Pathology, College of Veterinary Medicine, Kyungpook National University, Daegu, Buk-ku 702-701, Republic of Korea.
authors.forename: Moon-Jung
authors.initials: MJ
authors.lastname: Goo
authors.forename: Mi-Ran
authors.initials: MR
authors.lastname: Ki
authors.forename: Hye-Rim
authors.initials: HR
authors.lastname: Lee
authors.forename: Hai-Jie
authors.initials: HJ
authors.lastname: Yang
authors.forename: Dong-Wei
authors.initials: DW
authors.lastname: Yuan
authors.forename: Il-Hwa
authors.initials: IH
authors.lastname: Hong
authors.forename: Jin-Kyu
authors.initials: JK
authors.lastname: Park
authors.forename: Kyung-Sook
authors.initials: KS
authors.lastname: Hong
authors.forename: Jung-Youn
authors.initials: JY
authors.lastname: Han
authors.forename: Ok-Kyung
authors.initials: OK
authors.lastname: Hwang
authors.forename: Dong-Hwan
authors.initials: DH
authors.lastname: Kim
authors.forename: Sun-Hee
authors.initials: SH
authors.lastname: Do
authors.forename: Ronald D
authors.initials: RD
authors.lastname: Cohn
authors.forename: Kyu-Shik
authors.initials: KS
authors.lastname: Jeong
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism; D002251:Carbon Tetrachloride / Q000633:toxicity; D018450:Disease Progression; D015964:Gene Expression Regulation, Bacterial; D016481:Helicobacter Infections / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics / Q000472:pathogenicity*; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental / Q000097:blood / Q000382:microbiology* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D015415:Biomarkers; D002135:Calcium-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; D012336:RNA, Ribosomal, 16S; C513324:Rgn protein, mouse; D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase