Evidence map›Paper›PMID 25334003›Full record

ArticlePloS one2014

Infection with Porphyromonas gingivalis exacerbates endothelial injury in obese mice.

Min Ao, Mutsumi Miyauchi, Toshihiro Inubushi, Masae Kitagawa, Hisako Furusho, Toshinori Ando, Nurina Febriyanti Ayuningtyas, Atsuhiro Nagasaki, Kazuyuki Ishihara, Hidetoshi Tahara and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.5field-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

19 citing papers in PubMed, 45 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Min AoDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan; Department of Pediatric Dentistry, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Mutsumi MiyauchiDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Toshihiro InubushiDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Masae KitagawaCenter of Oral Clinical Examination, Hiroshima University Hospital, Hiroshima University, Hiroshima, Japan.
Hisako FurushoDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Toshinori AndoDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Nurina Febriyanti AyuningtyasDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Atsuhiro NagasakiDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kazuyuki IshiharaDepartment of Microbiology, Tokyo Dental College, Tokyo, Japan.
Hidetoshi TaharaDepartment of Cellular and Molecular Biology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Katsuyuki KozaiDepartment of Pediatric Dentistry, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Takashi TakataDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroshima University · JPHiroshima University Hospital · JPTokyo Dental College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA number of studies have revealed a link between chronic periodontitis and cardiovascular disease in obese patients. However, there is little information about the influence of periodontitis-associated bacteria, Porphyromonas gingivalis (Pg), on pathogenesis of atherosclerosis in obesity.

methodsIn vivo experiment: C57BL/6J mice were fed with a high-fat diet (HFD) or normal chow diet (CD), as a control. Pg was infected from the pulp chamber. At 6 weeks post-infection, histological and immunohistochemical analysis of aortal tissues was performed. In vitro experiment: hTERT-immortalized human umbilical vein endothelial cells (HuhT1) were used to assess the effect of Pg/Pg-LPS on free fatty acid (FFA) induced endothelial cells apoptosis and regulation of cytokine gene expression.

resultsWeaker staining of CD31 and increased numbers of TUNEL positive cells in aortal tissue of HFD mice indicated endothelial injury. Pg infection exacerbated the endothelial injury. Immunohistochemically, Pg was detected deep in the smooth muscle of the aorta, and the number of Pg cells in the aortal wall was higher in HFD mice than in CD mice. Moreover, in vitro, FFA treatment induced apoptosis in HuhT1 cells and exposure to Pg-LPS increased this effect. In addition, Pg and Pg-LPS both attenuated cytokine production in HuhT1 cells stimulated by palmitate.

conclusionsDental infection of Pg may contribute to pathogenesis of atherosclerosis by accelerating FFA-induced endothelial injury.

Indexed as

AnimalsAortaApoptosisCyclooxygenase 2Diet, High-FatDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, ObeseMuscle, SmoothPalmitatesPeriodontitisCyclooxygenase 2LipopolysaccharidesPalmitatesPlatelet Endothelial Cell Adhesion Molecule-1Ptgs2 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID25334003
PMCPMC4204882
OpenAlexW1967993020

What OpenQuestion holds

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LicenceCC BY
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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.