Evidence map›Paper›PMID 26033565›Full record

ArticleNeuroscience2015

Dysregulated TNFα promotes cytokine proteome profile increases and bilateral orofacial hypersensitivity.

F Ma, L Zhang, H S Oz, M Mashni, K N Westlund

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  7. ALPK1 missense pathogenic variant in five families leads to ROSAH syndrome, an ocular multisystem autosomal dominant disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2019
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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

5 authors at 1 institution in 1 country.

F MaDepartment of Physiology, College of Medicine, University of Kentucky, Lexington, KY 40536-0298, United States. Electronic address: fei.ma@uky.edu.
L ZhangDepartment of Physiology, College of Medicine, University of Kentucky, Lexington, KY 40536-0298, United States. Electronic address: lzhanh@email.uky.edu.
H S OzDepartment of Physiology, College of Medicine, University of Kentucky, Lexington, KY 40536-0298, United States. Electronic address: hoz2@email.uky.edu.
M MashniDepartment of Physiology, College of Medicine, University of Kentucky, Lexington, KY 40536-0298, United States. Electronic address: mark.mashni3@uky.edu.
K N WestlundDepartment of Physiology, College of Medicine, University of Kentucky, Lexington, KY 40536-0298, United States. Electronic address: kwhigh2@uky.edu.
University of Kentucky · US

Funding

UKY DENTAL COBRE: POLYBACTERIAL PERIODONTITIS: N-3 PUFA AND ANTIOXIDANTSP20RR020145 · NCRR · UNIVERSITY OF KENTUCKY · PI ASHFORD, KRISTIN · 2004 to 2011
$18.3M
Peripheral and Central Pain Generators of Chronic Trigeminal Neuropathic PainI01BX002695 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI WESTLUND-HIGH, KARIN N. · 2016 to 2024
–
BLRD VA I01 BX002695NCRR NIH HHS P20 RR020145
6 · The paper itself

Abstract

backgroundTumor necrosis factor alpha (TNFα) is increased in patients with headache, neuropathic pain, periodontal and temporomandibular disease. This study and others have utilized TNF receptor 1/2 (TNFR1/2) knockout (KO) animals to investigate the effect of TNFα dysregulation in generation and maintenance of chronic neuropathic pain. The present study determined the impact of TNFα dysregulation in a trigeminal inflammatory compression (TIC) nerve injury model comparing wild-type (WT) and TNFR1/2 KO mice.

methodsChromic gut suture was inserted adjacent to the infraorbital nerve to induce the TIC model mechanical hypersensitivity. Cytokine proteome profiles demonstrated serology, and morphology explored microglial activation in trigeminal nucleus 10weeks post.

resultsTIC injury induced ipsilateral whisker pad mechanical allodynia persisting throughout the 10-week study in both TNFR1/2 KO and WT mice. Delayed mechanical allodynia developed on the contralateral whisker pad in TNFR1/2 KO mice but not in WT mice. Proteomic profiling 10weeks after chronic TIC injury revealed TNFα, interleukin-1alpha (IL-1α), interleukin-5 (IL-5), interleukin-23 (IL-23), macrophage inflammatory protein-1β (MIP-1β), and granulocyte-macrophage colony-stimulating factor (GM-CSF) were increased more than 2-fold in TNFR1/2 KO mice compared to WT mice with TIC. Bilateral microglial activation in spinal trigeminal nucleus was detected only in TNFR1/2 KO mice. p38 mitogen-activated protein kinase (MAPK) inhibitor and microglial inhibitor minocycline reduced hypersensitivity.

conclusionsThe results suggest the dysregulated serum cytokine proteome profile and bilateral spinal trigeminal nucleus microglial activation are contributory to the bilateral mechanical hypersensitization in this chronic trigeminal neuropathic pain model in the mice with TNFα dysregulation. Data support involvement of both neurogenic and humoral influences in chronic neuropathic pain.

Indexed as

AnimalsCytokinesDisease Models, AnimalFacial PainHot TemperatureHyperalgesiaMaleMice, 129 StrainMice, TransgenicMicrogliaProteomeReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITouchTrigeminal Nerve InjuriesTumor Necrosis Factor-alphaCytokinesProteomeReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITnfrsf1a protein, mouseTumor Necrosis Factor-alphaMAPKmechanical allodyniamicrogliaminocyclineneuropathic paintrigeminal inflammatory compression

Identifiers

PMID26033565
PMCPMC6201243
OpenAlexW434168887

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.