Evidence map›Paper›PMID 22110637›Full record

ArticlePloS one2011

Tobacco smoke augments Porphyromonas gingivalis-Streptococcus gordonii biofilm formation.

Juhi Bagaitkar, Carlo A Daep, Carol K Patel, Diane E Renaud, Donald R Demuth, David A Scott

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 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
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  12. Review
  13. Influence of Smoking on Periodontal and Implant Therapy: A Narrative Review.International journal of environmental research and public health · 2023
    Review
  14. Tobacco smoke exacerbates Filifactor alocis pathogenicity.Journal of clinical periodontology · 2023
    Article
  15. Review
  16. Article
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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

6 authors at 1 institution in 1 country.

Juhi BagaitkarDepartment of Microbiology and Immunology, University of Louisville, Louisville, Kentucky, United States of America.
Carlo A Daep
Carol K Patel
Diane E Renaud
Donald R Demuth
David A Scott
University of Louisville · US

Funding

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 DE019826NIDCR NIH HHS R01DE019826
6 · The paper itself

Abstract

Smoking is responsible for the majority of periodontitis cases in the US and smokers are more susceptible than non-smokers to infection by the periodontal pathogen Porphyromonas gingivalis. P. gingivalis colonization of the oral cavity is dependent upon its interaction with other plaque bacteria, including Streptococcus gordonii. Microarray analysis suggested that exposure of P. gingivalis to cigarette smoke extract (CSE) increased the expression of the major fimbrial antigen (FimA), but not the minor fimbrial antigen (Mfa1). Therefore, we hypothesized that CSE promotes P. gingivalis-S. gordonii biofilm formation in a FimA-dependent manner. FimA total protein and cell surface expression were increased upon exposure to CSE whereas Mfa1 was unaffected. CSE exposure did not induce P. gingivalis auto-aggregation but did promote dual species biofilm formation, monitored by microcolony numbers and depth (both, p<0.05). Interestingly, P. gingivalis biofilms grown in the presence of CSE exhibited a lower pro-inflammatory capacity (TNF-α, IL-6) than control biofilms (both, p<0.01). CSE-exposed P. gingivalis bound more strongly to immobilized rGAPDH, the cognate FimA ligand on S. gordonii, than control biofilms (p<0.001) and did so in a dose-dependent manner. Nevertheless, a peptide representing the Mfa1 binding site on S. gordonii, SspB, completely inhibited dual species biofilm formation. Thus, CSE likely augments P. gingivalis biofilm formation by increasing FimA avidity which, in turn, supports initial interspecies interactions and promotes subsequent high affinity Mfa1-SspB interactions driving biofilm growth. CSE induction of P. gingivalis biofilms of limited pro-inflammatory potential may explain the increased persistence of this pathogen in smokers. These findings may also be relevant to other biofilm-induced infectious diseases and conditions.

Indexed as

Bacterial ProteinsBiofilmsEnzymes, ImmobilizedFimbriae ProteinsGene Expression Regulation, BacterialGlyceraldehyde 3-Phosphate Dehydrogenase (NADP+)HumansInflammationNicotianaPorphyromonas gingivalisSmokeStreptococcus gordoniiUp-RegulationBacterial ProteinsEnzymes, ImmobilizedFimbriae ProteinsfimbrillinGlyceraldehyde 3-Phosphate Dehydrogenase (NADP+)Mfa1 protein, Porphyromonas gingivalisSmoke

Identifiers

PMID22110637
PMCPMC3215692
OpenAlexW2096030010

What OpenQuestion holds

Textmetadata
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.