Evidence map›Paper›PMID 23863904›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

IL-17 receptor A signaling is protective in infection-stimulated periapical bone destruction.

Emad AlShwaimi, Ellen Berggreen, Hisako Furusho, Jonathan Caleb Rossall, Justine Dobeck, Subbiah Yoganathan, Philip Stashenko, Hajime Sasaki

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 47 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

8 authors at 6 institutions in 6 countries.

Emad AlShwaimiDepartment of Restorative Dental Sciences, College of Dentistry, University of Dammam, 1982 Dammam, Saudi Arabia.
Ellen Berggreen
Hisako Furusho
Jonathan Caleb Rossall
Justine Dobeck
Subbiah Yoganathan
Philip Stashenko
Hajime Sasaki
Harvard University · USInstitute of Immunology · HRBioMimetic Systems (United States) · USDammam Central Hospital · SAInstitute of Animal Physiology of the Slovak Academy of Sciences · SKUniversity of Bergen · NO

Funding

REGULATION OF BONE DESTRUCTION IN PERIAPICAL LESIONSR01DE009018 · NIDCR · FORSYTH INSTITUTE · PI STASHENKO, PHILIP · 1989 to 2005
$1.5M
MicroCT Core Facility in the Forsyth InstituteS10RR027553 · NCRR · ADA FORSYTH INSTITUTE, INC. · PI SASAKI, HAJIME · 2010 to 2010
$295k
NCRR NIH HHS RR027553NCRR NIH HHS S10 RR027553NIDCR NIH HHS DE-09018NIDCR NIH HHS R01 DE009018
6 · The paper itself

Abstract

IL-17 is a pleiotropic cytokine produced by Th17 T cells that induces a myriad of proinflammatory mediators. However, different models of inflammation report opposite functional roles of IL-17 signal in terms of its effects on bone destruction. In this study we determined the role of IL-17RA signal in bone resorption stimulated by dentoalveolar infections. Infrabony resorptive lesions were induced by surgical pulp exposure and microbial infection of mouse molar teeth. IL-17 was strongly induced in periapical tissues in wild-type (WT) mice by 7 d after the infection but was not expressed in uninfected mice. Dentoalveolar infections of IL-17RA knockout (KO) mice demonstrated significantly increased bone destruction and more abscess formation in the apical area compared with WT mice. Infected IL-17RA KO mice exhibited significantly increased neutrophils and macrophages compared with the WT littermates at day 21, suggesting a failure of transition from acute to chronic inflammation in the IL-17RA KO mice. The expression of IL-1 (both α and β isoforms) and MIP2 were significantly upregulated in the IL-17RA KO compared with WT mice at day 21 postinfection. The development of periapical lesions in IL-17RA KO mice was significantly attenuated by neutralization of IL-1β and MIP2. Taken together, these results demonstrate that IL-17RA signal seems to be protective against infection-induced periapical inflammation and bone destruction via suppression of neutrophil and mononuclear inflammation.

Indexed as

Alveolar Bone LossAnimalsBone ResorptionChemokine CXCL2Chronic DiseaseCoinfectionCytokinesGene Expression RegulationInterleukin-17Interleukin-1alphaInterleukin-1betaMacrophages, PeritonealMaleMandibleMiceMice, Inbred C57BLChemokine CXCL2Cxcl2 protein, mouseCytokinesIl17ra protein, mouseInterleukin-17Interleukin-1alphaInterleukin-1betaReceptors, Interleukin-17

Identifiers

PMID23863904
PMCPMC3767040
OpenAlexW2140342647

What OpenQuestion holds

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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.