Evidence map›Paper›PMID 21181444›Full record

ArticleDigestive diseases and sciences2011

Role of cagA-positive Helicobacter pylori on cell proliferation, apoptosis, and inflammation in biliary cells.

Wongwarut Boonyanugomol, Chariya Chomvarin, Seung-Chul Baik, Jea-Young Song, Chariya Hahnvajanawong, Kyung-Mi Kim, Myung-Je Cho, Woo-Kon Lee, Hyung-Lyun Kang, Kwang-Ho Rhee and 1 more

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. The association of the advanced lung cancer inflammation index with the risk ofFrontiers in cellular and infection microbiology · 2026
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  7. Beyond the stomach: the association betweenFrontiers in cellular and infection microbiology · 2025
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  8. International journal of biological sciences · 2024
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  12. Review
  13. Infection withPathogens (Basel, Switzerland) · 2020
    Article
  14. Frontiers in medicine · 2020
    Article
  15. Review
  16. Frontiers in cellular and infection microbiology · 2017
    Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 4 countries.

Wongwarut BoonyanugomolDepartment of Microbiology, and Liver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. kong_55@hotmail.com
Chariya Chomvarin
Seung-Chul Baik
Jea-Young Song
Chariya Hahnvajanawong
Kyung-Mi Kim
Myung-Je Cho
Woo-Kon Lee
Hyung-Lyun Kang
Kwang-Ho Rhee
Banchob Sripa
Khon Kaen University · THGyeongsang National University · KRNational University College · PRNew Generation University College · ET

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsThe pathogenesis of Helicobacter pylori in the human hepatobiliary system has not been clearly elucidated. We compared the effects of H. pylori cagA(+) and cagA(-) mutant strains on cell proliferation, apoptosis, and inflammation in a cholangiocarcinoma (CCA) cell line (KKU-100).

methodsMTT and BrdU were used to determine cell viability and DNA synthesis, respectively. The results were further investigated by RT-PCR and Western-blot analysis. The production of interleukin-8 (IL-8) was measured by ELISA assay.

resultsAt low H. pylori inocula (cell-bacteria ratio of 1:1), the H. pylori cagA(+) strain showed a significant stimulation in KKU-100 cell growth (109 ± 1.79%) and DNA synthesis (131 ± 3.39%) than did the H. pylori cagA(-) strain (95 ± 3.06% and 120 ± 2.32%, respectively), through activation of the anti-apoptotic bcl-2 gene, MAP kinase and NF- κB cascade. By contrast, at high H. pylori inocula (cell-bacteria ratio of 1:200), the H. pylori cagA(+) strain showed a significant reduction in KKU-100 cell survival (49 ± 2.47%) and DNA synthesis (49 ± 1.14%) than did the H. pylori cagA(-) strain (60 ± 1.30% and 75 ± 4.00%, respectively), by increased iNOS, p53 and bax, while decreased bcl-2. Additionally, caspase-8 and -3 protein were activated. The H. pylori cagA (+) strain had significantly stronger effect on IL-8 production than did the cagA(-) strain.

conclusionsThese results suggest that the H. pylori cagA(+) strain may play an important role in the development of biliary cancer by disturbing cell proliferation, apoptosis, and promoting cell inflammation in the CCA cell line.

Indexed as

ApoptosisCell ProliferationInflammationAntigens, BacterialBacterial ProteinsBiliary TractCell Line, TumorDNAGene Expression RegulationHelicobacter pyloriHumansInterleukin-8Nitric Oxide Synthase Type IIVirulenceAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriDNAInterleukin-8Nitric Oxide Synthase Type II

Identifiers

PMID21181444
OpenAlexW2037200031

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.