Evidence map›Paper›PMID 21789261›Full record

ArticlePloS one2011

Concurrent proinflammatory and apoptotic activity of a Helicobacter pylori protein (HP986) points to its role in chronic persistence.

Ayesha Alvi, Suhail A Ansari, Nasreen Z Ehtesham, Mohammed Rizwan, Savita Devi, Leonardo A Sechi, Insaf A Qureshi, Seyed E Hasnain, Niyaz Ahmed

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. Dysregulated macrophage immunity inFrontiers in immunology · 2025
    Review
  2. FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025
    Review
  3. Article
  4. BioMed research international · 2019
    Review
  5. β-Defensins in the Fight against Helicobacter pylori.Molecules (Basel, Switzerland) · 2017
    Review
  6. Article
  7. Frontiers in cellular and infection microbiology · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Immune evasion strategies used by Helicobacter pylori.World journal of gastroenterology · 2014
    Review
  12. Helicobacter pylori and gastric cancer: Indian enigma.World journal of gastroenterology · 2014
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Epidemiology and pattern of antibiotic resistance in Helicobacter pylori: scenario from Saudi Arabia.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association
    Review
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

9 authors at 4 institutions in 3 countries.

Ayesha AlviInstitute of Life Sciences, University of Hyderabad Campus, Gachibowli, Hyderabad, India.
Suhail A Ansari
Nasreen Z Ehtesham
Mohammed Rizwan
Savita Devi
Leonardo A Sechi
Insaf A Qureshi
Seyed E Hasnain
Niyaz Ahmed
University of Hyderabad · INInstitute of Life Sciences · INUniversity of Malaya · MYUniversity of Sassari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori induces cytokine mediated changes in gastroduodenal pathophysiology, wherein, the activated macrophages at the sub-mucosal space play a central role in mounting innate immune response against the antigens. The bacterium gains niche through persistent inflammation and local immune-suppression causing peptic ulcer disease or chronic gastritis; the latter being a significant risk factor for the development of gastric adenocarcinoma. What favors persistence of H. pylori in the gastric niches is not clearly understood. We report detailed characterization of a functionally unknown gene (HP986), which was detected in patient isolates associated with peptic ulcer and gastric carcinoma. Expression and purification of recombinant HP986 (rHP986) revealed a novel, ∼29 kDa protein in biologically active form which associates with significant levels of humoral immune responses in diseased individuals (p<0.001). Also, it induced significant levels of TNF-α and Interleukin-8 in cultured human macrophages concurrent to the translocation of nuclear transcription factor-κB (NF-κB). Further, the rHP986 induced apoptosis of cultured macrophages through a Fas mediated pathway. Dissection of the underlying signaling mechanism revealed that rHP986 induces both TNFR1 and Fas expression to lead to apoptosis. We further demonstrated interaction of HP986 with TNFR1 through computational and experimental approaches. Independent proinflammatory and apoptotic responses triggered by rHP986 as shown in this study point to its role, possibly as a survival strategy to gain niche through inflammation and to counter the activated macrophages to avoid clearance.

Indexed as

ApoptosisAmino Acid SequenceBacterial Proteinsfas ReceptorGastrointestinal DiseasesGenetic LociHelicobacter InfectionsHelicobacter pyloriHumansImmunity, HumoralInflammation MediatorsInterleukin-8Models, BiologicalMolecular Sequence DataNF-kappa BProtein BindingBacterial ProteinsFAS protein, humanfas ReceptorInflammation MediatorsInterleukin-8NF-kappa BReceptors, Tumor Necrosis Factor, Type IRecombinant ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID21789261
PMCPMC3137634
OpenAlexW2130001850

What OpenQuestion holds

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LicenceCC BY
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.