Evidence map›Paper›PMID 31581596›Full record

ArticleJournal of clinical medicine2019

TREM-1 Is Upregulated in Experimental Periodontitis, and Its Blockade Inhibits IL-17A and RANKL Expression and Suppresses Bone loss.

Nagihan Bostanci, Toshiharu Abe, Georgios N Belibasakis, George Hajishengallis

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2019. 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
1.7field-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.

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  5. Therapeutic delivery of CCL2 modulates immune response and restores host-microbe homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

4 authors at 2 institutions in 3 countries.

Nagihan BostanciDivision of Oral Diseases, Department of Dental Medicine, Karolinska Institutet, 14104 Huddinge, Sweden. nagihan.bostanci@ki.se.
Toshiharu AbeDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. toshiharu@ikeshita-abeshika.com.
Georgios N BelibasakisDivision of Oral Diseases, Department of Dental Medicine, Karolinska Institutet, 14104 Huddinge, Sweden. george.belibasakis@ki.se.ORCID 0000-0002-8164-0653
George HajishengallisDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. geoh@upenn.edu.ORCID 0000-0001-7392-8852
University of Pennsylvania · USUniversity of Zurich · CH

Funding

P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Local endogenous regulators of functional immune plasticity in the periodontiumR37DE026152 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2016 to 2025
$3.5M
Neutrophil homeostasis and periodontitis: Novel concepts and treatmentsR01DE024153 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2016 to 2020
$2.0M
Del-1: Molecular and Cellular Targets in PeriodontitisR01DE024716 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2015 to 2019
$2.0M
NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE024153NIDCR NIH HHS R01 DE024716NIDCR NIH HHS R37 DE026152NIH HHS DE015254, DE024716, DE024153,DE026152Vetenskapsrådet 2017-01198
6 · The paper itself

Abstract

aimTriggering receptor expressed on myeloid cells-1 (TREM-1) is a modifier of local and systemic inflammation. There is clinical evidence implicating TREM-1 in the pathogenesis of periodontitis. However, a cause-and-effect relationship has yet to be demonstrated, as is the underlying mechanism. The aim of this study was to elucidate the role of TREM-1 using the murine ligature-induced periodontitis model.

methodsA synthetic antagonistic LP17 peptide or sham control was microinjected locally into the palatal gingiva of the ligated molar teeth.

resultsMice treated with the LP17 inhibitor developed significantly less bone loss as compared to sham-treated mice, although there were no differences in total bacterial load on the ligatures. To elucidate the impact of LP17 on the host response, we analyzed the expression of a number of immune-modulating genes. The LP17 peptide altered the expression of 27/92 genes ≥ two-fold, but only interleukin (IL)-17A was significantly downregulated (4.9-fold). Importantly, LP17 also significantly downregulated the receptor activator of nuclear factor kappa-B-ligand (RANKL) to osteoprotegerin (OPG) ratio that drives osteoclastic bone resorption in periodontitis.

conclusionOur findings show for the first time that TREM-1 regulates the IL-17A-RANKL/OPG axis and bone loss in experimental periodontitis, and its therapeutic blockade may pave the way to a novel treatment for human periodontitis.

Indexed as

IL-17inflammationinterventionLP17OPGperiodontal diseaseRANKLTREM-1

Identifiers

PMID31581596
PMCPMC6832657
OpenAlexW2977910134

What OpenQuestion holds

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Registered trials

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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.