Evidence map›Paper›PMID 11254631›Full record

ArticleInfection and immunity2001

Proinflammatory and proapoptotic activities associated with Bordetella pertussis filamentous hemagglutinin.

T Abramson, H Kedem, D A Relman

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Filamentous Hemagglutinin ofInternational journal of molecular sciences · 2022
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Hemolytic uremic syndrome caused by Bordetella pertussis infection.Pediatric nephrology (Berlin, Germany) · 2010
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Hemolytic uremic syndrome in an infant following Bordetella pertussis infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2006
    Article
  20. Bordetella filamentous hemagglutinin plays a critical role in immunomodulation, suggesting a mechanism for host specificity.Proceedings of the National Academy of Sciences of the United States of America · 2005
    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

3 authors at 1 institution in 1 country.

T AbramsonDepartment of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.
H Kedem
D A Relman
Stanford University · US

Funding

BORDETELLA PERTUSSIS AND MONOCYTE INTEGRIN RECEPTORSR01AI039587 · NIAID · STANFORD UNIVERSITY · PI RELMAN, DAVID A · 1997 to 2001
$401k
NIAID NIH HHS R01 AI39587
6 · The paper itself

Abstract

Filamentous hemagglutinin (FHA) is a dominant cell surface-associated Bordetella pertussis adhesin. Recognition that this protein is secreted in significant amounts and that bacterial adhesins may have other activities, prompted an assessment of FHA effects on human macrophages. Incubation of human macrophage-like U937 cells with preparations of FHA resulted in dose-dependent cytotoxicity, with death of 95% of treated cells after 24 h. Based on the use of four independent methods, death of these cells could be largely attributed to apoptosis. FHA-associated apoptosis was also observed in THP-1 macrophage-like cells, fresh human peripheral blood monocyte-derived macrophages (MDM), and BEAS-2B human bronchial epithelial cells. Infection of MDM with wild-type B. pertussis resulted in apoptosis within 6 h, while infection with an FHA-deficient derivative strain was only 50% as effective. FHA-associated cytotoxicity was preceded by host cell secretion of tumor necrosis factor alpha (TNF-alpha), a potential proapoptotic factor. However, pretreatment of cells with a neutralizing anti-TNF-alpha monoclonal antibody inhibited only 16% of the FHA-associated apoptosis. On the other hand, a blocking monoclonal antibody directed against TNF-alpha receptor 1 inhibited FHA-associated apoptosis by 47.7% (P = 0.0001), suggesting that this receptor may play a role in the death pathway activated by FHA. Our in vitro data indicate that secreted and cell-associated FHA elicits proinflammatory and proapoptotic responses in human monocyte-like cells, MDM, and bronchial epithelial cells and suggest a previously unrecognized role for this prominent virulence factor in the B. pertussis-host interaction.

Indexed as

Virulence Factors, BordetellaAdhesins, BacterialApoptosisBacterial AdhesionBordetella pertussisCell LineDose-Response Relationship, DrugHemagglutininsHumansInflammationLipopolysaccharidesTumor Necrosis Factor-alphaVirulenceAdhesins, Bacterialfilamentous hemagglutinin adhesin, Bordetella pertussisHemagglutininsLipopolysaccharidesTumor Necrosis Factor-alphaVirulence Factors, Bordetella

Identifiers

PMID11254631
PMCPMC98203
OpenAlexW2097490488

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.