Evidence map›Paper›PMID 28912533›Full record

ArticleScientific reports2017

Oral fibroblasts modulate the macrophage response to bacterial challenge.

Rinat Tzach-Nahman, Rizan Nashef, Omer Fleissig, Aharon Palmon, Lior Shapira, Asaf Wilensky, Gabriel Nussbaum

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 34 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

7 authors at 1 institution in 1 country.

Rinat Tzach-NahmanThe Institute of Dental Sciences, the Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel.
Rizan NashefThe Department of Oral and Maxillofacial Surgery, the Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel.
Omer FleissigThe Institute of Dental Sciences, the Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel.
Aharon PalmonThe Institute of Dental Sciences, the Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel.
Lior ShapiraThe Department of Periodontology, the Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel.ORCID 0000-0001-9145-5155
Asaf WilenskyThe Department of Periodontology, the Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel.
Gabriel NussbaumThe Institute of Dental Sciences, the Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel. gabrieln@ekmd.huji.ac.il.
Hebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue damage in chronic periodontal disease is driven by the host response to a dysbiotic microbiota, and not by bacteria directly. Among chronic inflammatory diseases of the oral cavity, inflammation and tissue damage around dental implants (peri-implantitis) is emerging as a major clinical challenge, since it is more severe and less responsive to treatment compared to inflammation around natural teeth. We tested whether oral fibroblasts from the periodontal ligament (PDLF), which are present around natural teeth but not around dental implants, actively regulate inflammatory responses to bacterial stimulation. We show that human PDLF down-regulate TNF-α post-transcriptionally in macrophages stimulated with the oral pathogen Porphyromonas gingivalis. Cell contact and secretion of IL-6 and IL-10 contribute to the modulation of inflammatory cytokine production. Although fibroblasts decreased TNF-α secretion, they enhanced the ability of macrophages to phagocytose bacteria. Surprisingly, donor matched oral fibroblasts from gingival tissues, or fibroblasts from peri-implant inflamed tissues were at least as active as PDLF in regulating macrophage responses to bacteria. In addition, priming fibroblasts with inflammatory mediators enhanced PDLF regulatory activity. A further understanding of the spectrum of fibroblast activities in inflammatory lesions is important in order to design ways to control inflammatory tissue damage.

Indexed as

Cell CommunicationCell LineFibroblastsHumansInterleukin-10Interleukin-6MacrophagesPhagocytosisPorphyromonas gingivalisTumor Necrosis Factor-alphaIL10 protein, humanIL6 protein, humanInterleukin-10Interleukin-6Tumor Necrosis Factor-alpha

Identifiers

PMID28912533
PMCPMC5599598
OpenAlexW2754780576

What OpenQuestion holds

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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.