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- Abu Al-Soud, Waleed, et al.
(författare)
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DNA of Helicobacter spp. and common gut bacteria in primary liver carcinoma.
- 2008
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Ingår i: Digestive and Liver Disease. - : Elsevier BV. - 1590-8658. ; 40:2, s. 126-131
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIM: Gastric and enteric Helicobacter species have been associated with the pathogenesis of some extragastric diseases. METHODS: We retrospectively investigated the presence of DNA of Helicobacter species in samples of the cancer and the surrounding tumour-free liver tissues of patients with hepatocellular carcinoma (HCC, n=12) and cholangiocarcinoma (CC, n=13). The patients were from an area with low liver cancer incidence and with low hepatitis B and C prevalence. Patients with a benign liver disease (n=24) were included as controls. Paraffin-embedded liver samples were examined by a Helicobacter genus-specific PCR assay as well as group-specific PCR assays for Enterobacteriaceae, Bacteroides, Lactobacillus and Enterococcus. PCR products of positive samples were characterised by denaturing gradient gel electrophoresis (DGGE) and DNA sequencing. RESULTS: PCR assay detected Helicobacter DNA in seven of 12 (58%) and eight of 13 (62%) normal liver tissue specimens from HCC and CC patients, respectively. Two cancer samples from HCC patients were Helicobacter-positive but none of the CC cancers. In the control group, three of 24 (12.5%) patients with a benign liver condition were positive for Helicobacter species (p<0.01 compared to results of tumour-free liver tissue from the cancer patients). DGGE and DNA sequence analysis showed that 90% of the detected PCR products were "H. pylori-like". DNA of some other enteric bacteria was detected in the liver of one cancer patient and one control (4% of all patients). CONCLUSION: The presence of DNA of Helicobacter species in liver specimens, but not of other common gut bacteria, was associated with human hepatic carcinogenesis.
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| 2. |
- Casswall, TH, et al.
(författare)
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Bovine anti-Helicobacter pylori antibodies for oral immunotherapy
- 2002
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 37:12, s. 1380-1385
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Tidskriftsartikel (refereegranskat)abstract
- Background: Passive immunization with orally administered antibodies against specific pathogens has previously been successfully used therapeutically in both animal and human studies. We employed a similar strategy for experimental treatment of mice infected with the gastric pathogen Helicobacter pylori. Methods: An anti-H. pylori bovine colostral hyperimmune immunoglobulin preparation (BIC) was generated and its efficacy was tested in different in vitro experiments, such as binding to the Lewis(b) blood group antigen, inhibition of adherence of H. pylori to human gastric mucosa tissue sections in situ and in a haemagglutination assay. The BIC preparation was also given in the drinking water to H. pylori-infected mice. Results: An inhibition of 95% of the binding of H. pylori to Lewis(b) glycoconjugate was observed in vitro. Furthermore, a blocking activity of almost 90% was observed when the BIC was preincubated with H. pylori bacteria. Finally, the BIC preparation inhibited the haemagglutination of H. pylori and human red blood cells. Seven of 40 (17.5%) mice remained infected in the treatment group as compared with 25 of 45 (55.5%) in the control group. Hence, the cure rate was 66%, P = < 0.001. The mean number of colonies in the antibody-treated mice where eradication was not successful was also reduced (P < 0.05). In trials using FVB/N transgenic Lewis(b) expressing mice, a cure rate of 50%-66% was observed. Conclusion: Bovine colostral antibodies against H. pylori can be generated in high titres, inhibit binding in vitro and can eradicate or reduce the number of bacteria in infected mice.
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| 3. |
- Friis-Hansen, Lennart, et al.
(författare)
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Gastric inflammation, metaplasia, and tumor development in gastrin-deficient mice
- 2006
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Ingår i: Gastroenterology. - : Elsevier BV. - 1528-0012 .- 0016-5085. ; 131:1, s. 246-258
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: Gastrin deficiency and proton pump inhibitor treatment cause achlorhydria, which predisposes to disease. To elucidate the underlying molecular biology, we examined the changes in gastric gene expression in both types of achlorhydria. We also explored the associated changes in the gastric microflora and the long-term consequences of gastrin-deficient achlorhydria. Methods: Expression profiles were generated from gastric RNA from wild-type mice, gastrin knockout (KO) mice, gastrin KO mice after I week of gastrin infusion, and wild-type mice treated for I month with a proton pump inhibitor. The results were confirmed using real-time polymerase chain reaction and immuno-histochemistry. Selective media were used to characterize the gastric microflora. Results: The number of gastric bacteria was increased in both gastrin KO and PPI-treated mice. The expression profiles revealed activation of immune defense genes, interferon-regulated response genes, and intestinal metaplasia of the gastric mucosa. In young gastrin-deficient mice, gastrin infusions reversed the changes. Over time, the changes accumulated, became irreversible, and progressed into metaplasia and polyp development. Finally, the study showed that gastrin regulated the expression of genes encoding extracellular matrix proteins. Conclusions: Independently of gastrin, achlorhydria is associated with gastric bacterial overgrowth and intestinal gene expression patterns and is associated with predisposition to disease. Gastrin is therefore essential for prevention of gastric disease, mainly through control of acid secretion but to a lesser extent also through control of gastric gene expression. The gastrin-deficient mouse serves as a useful new model for gastric metaplasia and neoplasia.
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