ArticlePloS one2013
Helicobacter pylori cag pathogenicity island (cagPAI) involved in bacterial internalization and IL-8 induced responses via NOD1- and MyD88-dependent mechanisms in human biliary epithelial cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Beyond the stomach: the association betweenFrontiers in cellular and infection microbiology · 2025Review
- Comparative genomics of two Vietnamese Helicobacter pylori strains, CHC155 from a non-cardia gastric cancer patient and VN1291 from a duodenal ulcer patient.Scientific reports · 2023Article
- Immunoinformatic prediction of potential immunodominant epitopes from cagW in order to investigate protection against Helicobacter pylori infection based on experimental consequences.Functional & integrative genomics · 2023Article
- Helicobacter Species and Hepato-Biliary Tract Malignancies: A Systematic Review and Meta-Analysis.Cancers · 2023Review
- Adherence ofParasitology · 2022Article
- Foodborne trematodes: old foes, new kids on the block and research perspectives for control and understanding host-parasite interactions.Parasitology · 2022Article
- Article
- From Tumor Cells to Endothelium and Gut Microbiome: A Complex Interaction Favoring the Metastasis Cascade.Frontiers in oncology · 2022Review
- Helicobacter pylori infection causes both protective and deleterious effects in human health and disease.Genes and immunity · 2021Review
- Infection withPathogens (Basel, Switzerland) · 2020Article
- Role of amoebae for survival and recovery of 'non-culturable' Helicobacter pylori cells in aquatic environments.FEMS microbiology ecology · 2020Article
- Article
- Complete genome sequence of Helicobacter pylori B128 7.13 and a single-step method for the generation of unmarked mutations.Helicobacter · 2019Article
- Linking Helicobacter pylori with gallbladder and biliary tract cancer in Moroccan population using clinical and pathological profiles.Bioinformation · 2019Article
- Detection and genotyping of Helicobacter pylori in saliva versus stool samples from asymptomatic individuals in Northeastern Thailand reveals intra-host tissue-specific H. pylori subtypes.BMC microbiology · 2018Article
- Outer Membrane Vesicles From Probiotic and CommensalFrontiers in microbiology · 2018Article
- Co-infections with liver fluke and Helicobacter species: A paradigm change in pathogenesis of opisthorchiasis and cholangiocarcinoma?Parasitology international · 2017Review
- Elevated prevalence of Helicobacter species and virulence factors in opisthorchiasis and associated hepatobiliary disease.Scientific reports · 2017Article
- Genome-wide screen identified let-7c/miR-99a/miR-125b regulating tumor progression and stem-like properties in cholangiocarcinoma.Oncogene · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori infection has been proposed to be associated with various diseases of the hepatobiliary tract, including cancer of the bile duct epithelial cells (cholangiocarcinoma, CCA). The ability of H. pylori bacteria to cause pathogenic effects in these cells has, however, yet to be investigated. Given that the cag pathogenicity island (cagPAI) is required for H. pylori pathogenesis in gastric epithelial cells, we investigated wild-type and cag mutant strains for their ability to adhere, be internalized and induce pro-inflammatory responses in two bile duct epithelial cell lines derived from cases of CCA. The findings from these experiments were compared to results obtained with the well-characterized AGS gastric cancer cell line. We showed that the cagPAI encodes factors involved in H. pylori internalization in CCA cells, but not for adhesion to these cells. Consistent with previous studies in hepatocytes, actin polymerization and α5β1 integrin may be involved in H. pylori internalization in CCA cells. As for AGS cells, we observed significantly reduced levels of NF-κB activation and IL-8 production in CCA cells stimulated with either cagA, cagL or cagPAI bacteria, when compared with wild-type bacteria. Importantly, these IL-8 responses could be inhibited via either pre-treatment of cells with antibodies to α5β1 integrins, or via siRNA-mediated knockdown of the innate immune signaling molecules, nucleotide oligomerization domain 1 (NOD1) and myeloid differentiation response gene 88 (MyD88). Taken together, the data demonstrate that the cagPAI is critical for H. pylori pathogenesis in bile duct cells, thus providing a potential causal link for H. pylori in biliary tract disease.
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