Evidence map›Paper›PMID 15760449›Full record

ArticleCellular microbiology2005

Suppression of NF-kappaB-mediated beta-defensin gene expression in the mammalian airway by the Bordetella type III secretion system.

Diana Legarda, Marcia E Klein-Patel, Sunghan Yim, Ming H Yuk, Gill Diamond

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in cellular and infection microbiology · 2020
    Review
  4. Article
  5. Article
  6. Rediscovering Pertussis.Frontiers in pediatrics · 2016
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Stimulation of lung innate immunity protects against lethal pneumococcal pneumonia in mice.American journal of respiratory and critical care medicine · 2008
    Article
  14. Article
  15. Induction of cathelicidin in normal and CF bronchial epithelial cells by 1,25-dihydroxyvitamin D(3).Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2007
    Article
  16. Review
  17. Article
  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

5 authors at 2 institutions in 1 country.

Diana LegardaDepartment of Oral Biology, UMDNJ - New Jersey Dental School, Newark, NJ, USA.
Marcia E Klein-Patel
Sunghan Yim
Ming H Yuk
Gill Diamond
Rutgers, The State University of New Jersey · USUniversity of Pennsylvania · US

Funding

Bacteria-host cell interactions in periodontal diseaseR01DE014897 · NIDCR · UNIV OF MED/DENT OF NJ-NJ DENTAL SCHOOL · PI DIAMOND, GILL · 2002 to 2005
$1.6M
Type III Secretion in Bordetella PathogenesisR01AI049346 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI YUK, MING H. · 2002 to 2006
$1.4M
Host-Pathogen Interactions in the Mammalian AirwayR01HL067871 · NHLBI · UNIV OF MED/DENT OF NJ-NJ DENTAL SCHOOL · PI DIAMOND, GILL · 2003 to 2006
$1.2M
NHLBI NIH HHS R01 HL067871NHLBI NIH HHS R01 HL67871NIAID NIH HHS R01 AI049346NIDCR NIH HHS R01 DE014897NIDCR NIH HHS R01 DE14897
6 · The paper itself

Abstract

Expression of innate immune genes such as beta-defensins is induced in airway epithelium by bacterial components via activation of NF-kappaB. We show here that live Gram-negative bacteria can similarly stimulate this pathway, resulting in upregulation of the beta-defensin tracheal antimicrobial peptide (TAP) in primary cultures of bovine tracheal epithelial cells (TECs), by a Toll-like receptor 4 (TLR4)-mediated pathway. The Gram-negative airway pathogen Bordetella bronchiseptica possesses a type III secretion system previously suggested to inhibit the nuclear translocation of NF-kappaB in a cell line by immunohistochemistry. We therefore hypothesized that this pathogen might interfere in the innate immune response of the epithelium. Exposure of TECs to wild-type B. bronchiseptica suppressed the activation of NF-kappaB and the subsequent induction of TAP mRNA levels, whereas a type III secretion-defective strain did not. These results suggest a mechanism for bacterial evasion of the innate immune response in the airway, which could allow for the observed persistent colonization of this pathogen.

Indexed as

Gene Expression RegulationAnimalsAntimicrobial Cationic Peptidesbeta-DefensinsBordetella bronchisepticaCattleCells, CulturedEpithelial CellsMembrane GlycoproteinsNF-kappa BReceptors, Cell SurfaceToll-Like Receptor 4Toll-Like ReceptorsTracheaUp-RegulationAntimicrobial Cationic Peptidesbeta-DefensinsMembrane GlycoproteinsNF-kappa BReceptors, Cell SurfaceToll-Like Receptor 4Toll-Like Receptorstracheal antimicrobial peptide, bovine

Identifiers

PMID15760449
PMCPMC2111170
OpenAlexW1551023212

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.