Evidence map›Paper›PMID 19175666›Full record

ArticleEnvironmental microbiology2009

Tobacco-induced alterations to Porphyromonas gingivalis-host interactions.

Juhi Bagaitkar, Lisa R Williams, Diane E Renaud, Manjunatha R Bemakanakere, Mike Martin, David A Scott, Donald R Demuth

Open access · greenAbstract read
In one paragraph

Article in Environmental microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Influence of Smoking on Periodontal and Implant Therapy: A Narrative Review.International journal of environmental research and public health · 2023
    Review
  11. Tobacco smoke exacerbates Filifactor alocis pathogenicity.Journal of clinical periodontology · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Oral Osteomicrobiology: The Role of Oral Microbiota in Alveolar Bone Homeostasis.Frontiers in cellular and infection microbiology · 2021
    Review
  17. Review
  18. Review
  19. Review
  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

7 authors at 1 institution in 2 countries.

Juhi BagaitkarMicrobiology and Immunology, University of Louisville, Louisville, KY 40292, USA.
Lisa R Williams
Diane E Renaud
Manjunatha R Bemakanakere
Mike Martin
David A Scott
Donald R Demuth
Bipar · FR

Funding

Strategic Vision & Impact on Environmental HealthP30ES014443 · NIEHS · UNIVERSITY OF LOUISVILLE · PI PROUGH, RUSSELL ALLEN · 2007 to 2010
$4.4M
Tobacco-induced alterations to P. gingivalis-host interactionsR01DE019826 · NIDCR · UNIVERSITY OF LOUISVILLE · PI SCOTT, DAVID A · 2010 to 2014
$1.8M
NIDCR NIH HHS R01 DE019826NIEHS NIH HHS P30 ES014443NIEHS NIH HHS P30ES014443-01A1
6 · The paper itself

Abstract

Smokers are more susceptible than non-smokers to persistent infection by Porphyromonas gingivalis, a causative agent of periodontitis. Patients who smoke exhibit increased susceptibility to periodontitis and are more likely to display severe disease and be refractory to treatment. Paradoxically, smokers demonstrate reduced clinical inflammation. We show that P. gingivalis cells exposed to cigarette smoke extract (CSE) induce a lower proinflammatory response (tumour necrosis factor-alpha, interleukin-6, interleukin-12 p40) from monocytes and peripheral blood mononuclear cells than do unexposed bacteria. This effect is reversed when CSE-exposed bacteria are subcultured in fresh medium without CSE. Using microarrays representative of the P. gingivalis genome, CSE-exposure resulted in differential regulation of 6.8% of P. gingivalis genes, including detoxification and oxidative stress-related genes; DNA repair genes; and multiple genes related to P. gingivalis virulence, including genes in the major fimbrial and capsular operons. Exposure to CSE also altered the expression of outer membrane proteins, most notably by inducing the virulence factors RagA and RagB, and a putative lipoprotein cotranscribed with the minor fimbrial antigen. Therefore, CSE represents an environmental stress to which P. gingivalis adapts by altering gene expression and outer membrane proteins. These changes may explain, in part, the altered virulence and host-pathogen interactions that have been documented in vivo in smokers with periodontal disease.

Indexed as

Cell LineCells, CulturedCytokinesGene ExpressionGene Expression ProfilingGene Expression Regulation, BacterialHost-Parasite InteractionsHumansLeukocytes, MononuclearMonocytesPorphyromonas gingivalisSmokingStress, PhysiologicalCytokines

Identifiers

PMID19175666
PMCPMC2713102
OpenAlexW2079664839

What OpenQuestion holds

Textmetadata
LicenceTDM
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.