Evidence map›Paper›PMID 23766556›Full record

ArticleMediators of inflammation2013

Flavonoid naringenin: a potential immunomodulator for Chlamydia trachomatis inflammation.

Abebayehu N Yilma, Shree R Singh, Lisa Morici, Vida A Dennis

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.0field-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

23 citing papers in PubMed, 71 citations in OpenAlex.

  1. New Promising Routes in Peptic Ulcers: Toll-like Receptors and Semaphorins.Endocrine, metabolic & immune disorders drug targets · 2024
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  11. Naringenin mitigates antituberculosis drugs induced hepatic and renal injury in rats.Journal of traditional and complementary medicine · 2020
    Article
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  13. Review
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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 1 country.

Abebayehu N YilmaDepartment of Biological Sciences, Center for NanoBiotechnology and Life Sciences Research, Alabama State University, 1627 Hall Street, Montgomery, AL 36104, USA.
Shree R Singh
Lisa Morici
Vida A Dennis
Alabama State University · USTulane University · US

Funding

RISE Option II:NIGMS-Research Initiative for Scientific Enhancement (RISE) Program at ASUR25GM106995 · NIGMS · ALABAMA STATE UNIVERSITY · PI DENNIS, VIDA A · 2013 to 2023
$3.0M
NIGMS NIH HHS R25 GM106995
6 · The paper itself

Abstract

Chlamydia trachomatis, the agent of bacterial sexually transmitted infections, can manifest itself as either acute cervicitis, pelvic inflammatory disease, or a chronic asymptomatic infection. Inflammation induced by C. trachomatis contributes greatly to the pathogenesis of disease. Here we evaluated the anti-inflammatory capacity of naringenin, a polyphenolic compound, to modulate inflammatory mediators produced by mouse J774 macrophages infected with live C. trachomatis. Infected macrophages produced a broad spectrum of inflammatory cytokines (GM-CSF, TNF, IL-1β, IL-1α, IL-6, IL-12p70, and IL-10) and chemokines (CCL4, CCL5, CXCL1, CXCL5, and CXCL10) which were downregulated by naringenin in a dose-dependent manner. Enhanced protein and mRNA gene transcript expressions of TLR2 and TLR4 in addition to the CD86 costimulatory molecule on infected macrophages were modulated by naringenin. Pathway-specific inhibition studies disclosed that p38 mitogen-activated-protein kinase (MAPK) is involved in the production of inflammatory mediators by infected macrophages. Notably, naringenin inhibited the ability of C. trachomatis to phosphorylate p38 in macrophages, suggesting a potential mechanism of its attenuation of concomitantly produced inflammatory mediators. Our data demonstrates that naringenin is an immunomodulator of inflammation triggered by C. trachomatis, which possibly may be mediated upstream by modulation of TLR2, TLR4, and CD86 receptors on infected macrophages and downstream via the p38 MAPK pathway.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineChlamydia InfectionsChlamydia trachomatisFlavanonesFlow CytometryGranulocyte-Macrophage Colony-Stimulating FactorImmunologic FactorsInterleukin-10Interleukin-1alphaInterleukin-1betaInterleukin-6MacrophagesMicep38 Mitogen-Activated Protein KinasesAnti-Inflammatory AgentsFlavanonesGranulocyte-Macrophage Colony-Stimulating FactorImmunologic FactorsInterleukin-10Interleukin-1alphaInterleukin-1betaInterleukin-6naringeninp38 Mitogen-Activated Protein KinasesTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID23766556
PMCPMC3676976
OpenAlexW2081658596

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.