Co-infections with liver fluke and Helicobacter species: A paradigm change in pathogenesis of opisthorchiasis and cholangiocarcinoma?

Sripa, Banchob; Deenonpoe, Raksawan; Brindley, Paul J.

doi:10.1016/j.parint.2016.11.016

Cited by 42 publications

(30 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…To confirm that Cag A+ H. pylori can also induce a hummingbird-like phenotype of the cholangiocyte, a demonstration that H69 cells can be infected by the H. pylori, and the cagPAI is functional during the infection, as established by detection of phosphorylated CagA, would be needed [88][89][90]. The present findings supported the hypothesis that opisthorchiasis and H. pylori together may hasten or even synergize the malignant transformation of cholangiocytes [2,3,91]. By contrast, co-infections of Helicobacter species including H. pylori and some other helminths have generally been associated with diminished risk of H. pylori-associated gastric carcinoma [92][93][94].…”

Section: H Pylori Induces Anchorage-independent Colony Formationsupporting

confidence: 82%

“…These lesions derive not only from liver fluke infection but perhaps are in part the consequence of hepatobiliary tract infection with H. pylori. Helicobacter may transit from the stomach to the duodenum and enter the biliary tree through the duodenal papilla and ampulla of Vater [26,78], and indeed may be vectored there by the liver fluke, O. viverrini [1][2][3]. H. pylori-specific DNA sequences have been detected in CCA tumors and also from lesions diagnosed as cholecystitis/cholelithiasis in regions endemic for opisthorchiasis [5,11].…”

Section: H Pylori Induces Anchorage-independent Colony Formationmentioning

confidence: 99%

“…There is increasing evidence that the East Asian liver fluke Opisthorchis viverrini may serve as a reservoir of Helicobacter which, in turn, implicates Helicobacter in pathogenesis of opisthorchiasis-associated cholangiocarcinoma (CCA) [1][2][3][4][5]. The International Agency for Research on Cancer of the World Health Organization classifies infection with the liver flukes O. viverrini and Clonorchis sinensis as well as H. pylori as Group 1 carcinogens [6].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Infection with CagA⁺Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes

Thanaphongdecha

Speigh

Tanno

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

Recent reports suggest that the East Asian liver fluke Opisthorchis viverrini, which is implicated in pathogenesis of opisthorchiasis-associated cholangiocarcinoma, serves as a reservoir of Helicobacter pylori. The affected cholangiocytes that line the intrahepatic biliary tract are considered to be the cell of origin of this malignancy. Here, we investigated interactions among a human cholangiocyte cell line, H69, a CCA cell line CC-LP-1, CagA+ve Helicobacter pylori, and H. bilis bacilli. Exposure to increasing numbers of H. pylori at 0, 1, 10,100 bacteria per cholangiocyte cell induced phenotypic changes in the cultured cholangiocytes including profusion of thread-like filopodia and loss of cell-cell contact in a dose-dependent fashion. In parallel, changes in mRNA expression followed exposure to H. pylori, with increased expression of epithelial to mesenchymal transition (EMT) associated-factors including snail, slug, vimentin, matrix metalloprotease, zinc finger E-box-binding homeobox, and the cancer stem cell marker CD44. Transcription levels encoding the cell adhesion marker CD24 decreased. Analysis in real time using the xCELLigence system to quantify cell proliferation, migration and invasion revealed that exposure to ten to 50 of H. pylori stimulated migration of H69 cells and CC-LP-1 cells, a line derived form of a human cholangiocarcinoma, and invasion through an extracellular matrix. In addition, ten bacilli of CagA+ve H. pylori stimulated contact-independent colony establishment in soft agar. These findings support the hypothesis that infection with H. pylori can contribute to the malignant transformation of the biliary epithelium.

show abstract

Section: H Pylori Induces Anchorage-independent Colony Formationsupporting

confidence: 82%

Section: H Pylori Induces Anchorage-independent Colony Formationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Infection with CagA⁺Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes

Thanaphongdecha

Speigh

Tanno

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, given the insufficiency of these hypotheses to explain the occurrence of cancer in the smallest part of the parasitized patients, more recent studies explore the auxiliary role of gastric, colorectal, and urogenital microbiomes ( 15 – 19 ).…”

Section: Helminths and Human Cancersmentioning

confidence: 99%

Helminths and Cancers From the Evolutionary Perspective

2018

View full text Add to dashboard Cite

Helminths include free-living and parasitic Platyhelminthes and Nematoda which infect millions of people worldwide. Some Platyhelminthes species of blood flukes (Schistosoma haematobium, Schistosoma japonicum, and Schistosoma mansoni) and liver flukes (Clonorchis sinensis and Opisthorchis viverrini) are known to be involved in human cancers. Other helminths are likely to be carcinogenic. Our main goals are to summarize the current knowledge of human cancers caused by Platyhelminthes, point out some helminth and human biomarkers identified so far, and highlight the potential contributions of phylogenetics and molecular evolution to cancer research. Human cancers caused by helminth infection include cholangiocarcinoma, colorectal hepatocellular carcinoma, squamous cell carcinoma, and urinary bladder cancer. Chronic inflammation is proposed as a common pathway for cancer initiation and development. Furthermore, different bacteria present in gastric, colorectal, and urogenital microbiomes might be responsible for enlarging inflammatory and fibrotic responses in cancers. Studies have suggested that different biomarkers are involved in helminth infection and human cancer development; although, the detailed mechanisms remain under debate. Different helminth proteins have been studied by different approaches. However, their evolutionary relationships remain unsolved. Here, we illustrate the strengths of homology identification and function prediction of uncharacterized proteins from genome sequencing projects based on an evolutionary framework. Together, these approaches may help identifying new biomarkers for disease diagnostics and intervention measures. This work has potential applications in the field of phylomedicine (evolutionary medicine) and may contribute to parasite and cancer research.

show abstract

“…Since Kawaguchi et al [7] detected H. pylori in the gallbladder's mucosa of a patient with cholecystitis, it has been suggested a potential link between H. pylori infection and biliary tract carcinogenesis. In fact, clinical and epidemiological studies have reported an association between GBC, CC, and previous infection with H. pylori [8,9]. Kuroki et al [10] showed that epithelial proliferation is higher in biliary epithelium infected with Helicobacter compared to a control group.…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori and Biliary Tract Cancers: A Meta-Analysis

Cherif

Bouriat

Rais

et al. 2020

Canadian Journal of Infectious Diseases and Medical Microbiolog

View full text Add to dashboard Cite

Background. Helicobacter pylori is detected in various extragastric diseases, including biliary tract cancers. Besides, gallbladder cancers, extracholangiocarcinomas, and intracholangiocarcinomas are highly lethal cancers with limited survival due to their late diagnosis. Epidemiological data on Helicobacter pylori infection and biliary tract cancer have been contradictory. Aim. The aim of this study is to explore and evaluate the association between the Helicobacter pylori infection and biliary tract cancer. Materials and Methods. Systematic literature research was carried out to identify all eligible articles. All relevant publications from 2000 to 2019 were retrieved using comprehensive combinations of keywords. We used a random effects model to calculate pooled prevalence estimates, and 95% confidence intervals (CIs) for odds ratio were also calculated. Quantitative assessment of heterogeneity was explored by the chi-square test and was measured using I2. Results. Thirteen case-control studies published between 2001 and 2018 were included. The overall meta-analysis favoured a significant association between Helicobacter pylori infection and biliary tract cancer (OR, 2.57; 95% CI, 1.35–4.91; I2 = 58%). Geographic distribution-based subgroup analysis showed a higher prevalence of H. pylori in Asian and North American countries. Evidence supporting the higher presence of Helicobacter pylori in a cancer group was found by PCR. In another subgroup, the ORs were 4.18 (2.03, 8.58) in cholangiocarcinoma, 1.36 (0.34, 5.44) in gallbladder cancer, and 5.93 (1.89, 18.63) in other biliary tract cancers. Conclusion. This meta-analysis suggests that infection of the biliary tract with Helicobacter pylori is related to an increased risk of biliary tract cancers.

show abstract

Co-infections with liver fluke and Helicobacter species: A paradigm change in pathogenesis of opisthorchiasis and cholangiocarcinoma?

Cited by 42 publications

References 57 publications

Infection with CagA⁺Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes

Infection with CagA⁺Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes

Helminths and Cancers From the Evolutionary Perspective

Helicobacter pylori and Biliary Tract Cancers: A Meta-Analysis

Contact Info

Product

Resources

About

Co-infections with liver fluke and Helicobacter species: A paradigm change in pathogenesis of opisthorchiasis and cholangiocarcinoma?

Cited by 42 publications

References 57 publications

Infection with CagA+Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes

Infection with CagA+Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes

Helminths and Cancers From the Evolutionary Perspective

Helicobacter pylori and Biliary Tract Cancers: A Meta-Analysis

Contact Info

Product

Resources

About

Infection with CagA⁺Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes

Infection with CagA⁺Helicobacter pyloriinduces epithelial to mesenchymal transition in human cholangiocytes