Evidence map›Paper›PMID 19170127›Full record

ArticleThe Prostate2009

Il-1 beta-induced post-transition effect of NF-kappaB provides time-dependent wave of signals for initial phase of intrapostatic inflammation.

Eugene V Vykhovanets, Sanjeev Shukla, Gregory T MacLennan, Olena V Vykhovanets, Donald R Bodner, Sanjay Gupta

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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  15. Antagonists of growth hormone-releasing hormone (GHRH) reduce prostate size in experimental benign prostatic hyperplasia.Proceedings of the National Academy of Sciences of the United States of America · 2011
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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

6 authors at 2 institutions in 1 country.

Eugene V VykhovanetsDepartment of Urology, Case Western Reserve University, Case Medical Center & University Hospitals of Cleveland, Cleveland, Ohio 44106, USA.
Sanjeev Shukla
Gregory T MacLennan
Olena V Vykhovanets
Donald R Bodner
Sanjay Gupta
Case Western Reserve University · USUniversity Hospitals of Cleveland · US

Funding

Prostate Cancer Chemoprevention by ApigeninR01CA108512 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2004 to 2014
$2.4M
NCI NIH HHS R01 CA108512
6 · The paper itself

Abstract

objectiveOur previous findings have shown that systemic administration of interleukin (IL)-1 beta induces up-regulation of nuclear factor-kappa B (NF-kappaB) in mouse prostate tissue that may be responsible for leukocyte extravasation into prostate stroma. It has been hypothesized that NF-kappaB plays a role in the development of prostatitis, and that NF-kappaB activation might provide chemoattractive signals for leukocyte extravasation in the prostate.

methodsIL-1 beta was administrated intravenously, alone or with dexamethasone (Dex), to separate groups of C57BL/6J mice. Expression of NF-kappaB, chemoattractant receptors, and IL-17F in the prostates of the two groups of mice at various time periods following treatment was evaluated and compared.

resultsIL-1 beta administration up-regulated NF-kappaB/p65 activity in the mouse prostate. IL-1 beta administration promoted extravasation and accumulation of CD45+ mononuclear cells but not neutrophils in the mouse prostate stroma. IL-1 beta administration provided earlier (4 hr) CXCR1/IL-8RA receptor expression in mouse prostate as a first signal, inducing capillary homing, adhesion, and initial extravasation of mononuclear cells into the prostate tissue. IL-1 beta administration also induced relatively late (24 hr) up-regulation of VCAM1 in the endothelial cells of microvessels and of IL-17F in prostate epithelium and in stromal infiltrating leukocytes. Concomitant administration of Dex, a known NF-kappaB inhibitor, resulted in significantly down-regulated IL-1 beta-induced NF-kappaB/p65 activity, as well as reduced expression of chemokine receptors and IL-17F in mouse prostate tissue.

conclusionSystemic IL-1 beta administration induces NF-kappaB-responsive genes to promote aberrant NF-kappaB/p65 activity, which may be critical in the development of prostatitis through its role in the production of chemoattractant signals that promote extravasation and stromal accumulation of mononuclear cells (mainly by CXCR1/IL-8RA), and initiation of a new wave of pro-inflammatory signals favorable to chronic inflammation (mainly by IL-17F).

Indexed as

AnimalsDexamethasoneInflammationInterleukin-17Interleukin-1betaLymphocytesMaleMiceMice, Inbred C57BLNF-kappa BProstatic NeoplasmsReceptors, ChemokineDexamethasoneInterleukin-17Interleukin-1betaNF-kappa BReceptors, Chemokine

Identifiers

PMID19170127
PMCPMC2669895
OpenAlexW2013093771

What OpenQuestion holds

Textmetadata
LicenceTDM
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.