Detection of<i>Helicobacter</i>species in liver and stomach tissues of patients with chronic liver diseases using polymerase chain reaction-denaturing gradient gel electrophoresis and immunohistochemistry

Stalke, Piotr; Al‐Soud, Waleed Abu; Bielawski, Krzysztof Piotr; Bakowska, Alicja; H, Trocha; Stępiński, Jan; Wadström, Torkel

doi:10.1080/00365520510023251

Cited by 30 publications

(29 citation statements)

References 26 publications

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“…In our study, changes in LFC and LFT were not significantly different in HP eradicated group from controls who did not receive 1552 eradication treatment. This finding is somehow in accordance with the result of Stalke et al (1). They reported no correlation between LFT and identification of HP DNA in the liver biopsy samples of CLD patients.…”

Section: Discussion:-supporting

confidence: 83%

Helicobacter Pylori Eradication Effect on Liver Fat Content in Patient With Non-Alcoholic Fatty Liver Disease.

Arnaout¹

2017

IJAR

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Section: Discussion:-supporting

confidence: 83%

Helicobacter Pylori Eradication Effect on Liver Fat Content in Patient With Non-Alcoholic Fatty Liver Disease.

Arnaout¹

2017

IJAR

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“…Xuan et al [29] have detected the cagA gene in only 3 of 17 (17.6%) positive samples from patients with HCC. Stalke et al [30] have identified Helicobacter species in the liver and stomach tissue of Polish patients with CLD PCR denaturing gradient gel electrophoresis and immunohistochemistry. Their results have shown that H. pylori-like organisms appeared to dominate the gastric mucosa and liver tissue patients.…”

Section: Discussionmentioning

confidence: 99%

Detection of Helicobacter pylori in Paraffin-Embedded Specimens from Patients with Chronic Liver Diseases, Using the Amplification Method

et al. 2008

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Helicobacter DNA has been detected in the liver specimens of patients with various hepato-biliary diseases. The aim of this study was to investigate the presence of H. pylori DNA in the liver tissue of Iranian patients with chronic liver diseases (CLD). Genomic DNA was extracted from the paraffin sections of 46 liver biopsies of patients with CLD and 13 from patients with metastatic adenocarcinoma as a control group. Polymerase chain reaction (PCR) analysis was carried out using primers for H. pylori 16S rRNA and cagA genes. On analysis, 17 of the 46 patient samples were positive in H. pylori 16S rRNA PCR and 2 of the 13 were positive from the control group. None of the samples were positive for the cagA gene. This study showed the greater presence of H. pylori-like DNA in the liver samples from patients with CLD than in controls.

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“…Liver diseases in which Helicobacter sp. DNA has been detected include cirrhosis, hepatocellular carcinomas (HCC) [5][6][7][8][9][10], primary sclerosing cholangitis, and primary biliary cirrhosis [11]. Although the role of Helicobacter sp.…”

Section: Introductionmentioning

confidence: 99%

“…in hepatobiliary diseases in animals and humans [1][2][3][4]. Helicobacter DNA, or cross-reacting DNA, has been detected in hepatic tissues from both adults and children with and without liver disease [5][6][7][8][9][10][11][12]. Liver diseases in which Helicobacter sp.…”

Section: Introductionmentioning

confidence: 99%

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

et al. 2008

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Although Helicobacter pylori have been identified in the liver, the role of Helicobacter sp. in human liver diseases remains unclear. This study explored whether H. pylori were internalized and could persist in hepatocytes. The majority of an inoculum of H. pylori (1 × 10 7 colony forming units) adhered to hepatocytes. Using the gentamicin invasion assay we found that approximately 2% were internalized and persisted following passage for more than 2 months. Electron microscopy confirmed the presence of intracellular Helicobacter. The number of adherent or internalized H. pylori was significantly greater with hepatocytes than with gastric epithelial cells (P <0.05) and was also dependent on cag pathogenicity island (PAI), VacA, OipA, or BabA status. Transmission electron microscopy was used to confirm adherence and invasion of H. pylori into hepatocytes. Internalization of H. pylori was inhibited by antibodies to β1-integrin receptors, genistein, and cytochalasin D (P < 0.05) consistent with β1-integrin acting as a surface receptor with additional requirements for tyrosine kinase phosphorylation and actin polymerization. In summary, H. pylori both adhered to and invaded into hepatocytes in vitro, depending on the virulent factors, and persisted within hepatocytes during subcultures. β1-integrin is likely a receptor involved in internalization of H. pylori into hepatocytes.

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Detection ofHelicobacterspecies in liver and stomach tissues of patients with chronic liver diseases using polymerase chain reaction-denaturing gradient gel electrophoresis and immunohistochemistry

Cited by 30 publications

References 26 publications

Helicobacter Pylori Eradication Effect on Liver Fat Content in Patient With Non-Alcoholic Fatty Liver Disease.

Helicobacter Pylori Eradication Effect on Liver Fat Content in Patient With Non-Alcoholic Fatty Liver Disease.

Detection of Helicobacter pylori in Paraffin-Embedded Specimens from Patients with Chronic Liver Diseases, Using the Amplification Method

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

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