Evidence map›Paper›PMID 21342497›Full record

ArticleMolecular pain2011

Spinal toll like receptor 3 is involved in chronic pancreatitis-induced mechanical allodynia of rat.

Nian-Song Qian, Yong-Hui Liao, Quan-Xing Feng, Yu Tang, Ke-Feng Dou, Kai-Shan Tao

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Neural plasticity in pancreatitis and pancreatic cancer.Nature reviews. Gastroenterology & hepatology · 2015
    Review
  10. Molecular and cellular mechanisms that initiate pain and itch.Cellular and molecular life sciences : CMLS · 2015
    Review
  11. Article
  12. Article
  13. Spinal cord Toll-like receptor 4 mediates inflammatory and neuropathic hypersensitivity in male but not female mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
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 3 institutions in 2 countries.

Nian-Song QianDepartment of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, PR China.
Yong-Hui Liao
Quan-Xing Feng
Yu Tang
Ke-Feng Dou
Kai-Shan Tao
Xijing Hospital · CNAir Force Medical University · CNChinese People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMechanisms underlying pain in chronic pancreatitis (CP) are incompletely understood. Our previous data showed that astrocytes were actively involved. However, it was unclear how astrocytic activation was induced in CP conditions. In the present study, we hypothesized that toll-like receptors (TLRs) were involved in astrocytic activation and pain behavior in CP-induced pain.

resultsTo test our hypothesis, we first investigated the changes of TLR2-4 in the rat CP model induced by intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). Western blot showed that after TNBS infusion, TLR3, but not TLR2 or TLR4, was increased gradually and maintained at a very high level for up to 5 w, which correlated with the changing course of mechanical allodynia. Double immunostaining suggested that TLR3 was highly expressed on astrocytes. Infusion with TLR3 antisense oligodeoxynucleotide (ASO) dose-dependently attenuated CP-induced allodynia. CP-induced astrocytic activation in the spinal cord was also significantly suppressed by TLR3 ASO. Furthermore, real-time PCR showed that IL-1β, TNF-α, IL-6 and monocyte chemotactic protein-1 (MCP-1) were significantly increased in spinal cord of pancreatic rats. In addition, TLR3 ASO significantly attenuated CP-induced up-regulation of IL-1β and MCP-1.

conclusionsThese results suggest a probable "TLR3-astrocytes-IL-1β/MCP-1" pathway as a positive feedback loop in the spinal dorsal horn in CP conditions. TLR3-mediated neuroimmune interactions could be new targets for treating persistent pain in CP patients.

Indexed as

AnimalsBlotting, WesternChemokine CCL2HyperalgesiaInterleukin-1betaInterleukin-6MalePancreatitis, ChronicRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionSpinal CordToll-Like Receptor 3Tumor Necrosis Factor-alphaChemokine CCL2Interleukin-1betaInterleukin-6Toll-Like Receptor 3Tumor Necrosis Factor-alpha

Identifiers

PMID21342497
PMCPMC3048572
OpenAlexW1970047152

What OpenQuestion holds

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LicenceCC BY
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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.