Evidence map›Paper›PMID 18592153›Full record

ArticleJournal of gastroenterology2008

Pancreatic stellate cells express Toll-like receptors.

Atsushi Masamune, Kazuhiro Kikuta, Takashi Watanabe, Kennichi Satoh, Akihiko Satoh, Tooru Shimosegawa

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
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  6. Review
  7. Review
  8. Review
  9. Epigenetic Mechanisms of Pancreatobiliary Fibrosis.Current treatment options in gastroenterology · 2019
    Review
  10. The Orai CaThe Journal of physiology · 2019
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Biology of pancreatic stellate cells-more than just pancreatic cancer.Pflugers Archiv : European journal of physiology · 2017
    Review
  19. Review
  20. Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Review
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 1 institution in 1 country.

Atsushi MasamuneDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan.
Kazuhiro Kikuta
Takashi Watanabe
Kennichi Satoh
Akihiko Satoh
Tooru Shimosegawa
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundToll-like receptors (TLRs) are proteins involved in recognition of foreign pathogen-associated molecular patterns (PAMPs) and activation of innate immunity. This study aimed to clarify whether pancreatic stellate cells (PSCs), a major profibrogenic cell type in the pancreas, expressed TLRs and responded to PAMPs.

methodsPSCs were isolated from rat pancreas tissue, and expression of TLRs was examined. PSCs were treated with lipoteichoic acid (a ligand for TLR2), polyinosinic-polycytidylic acid (a ligand for TLR3), lipopolysaccharide (a ligand for TLR4), or flagellin (a ligand for TLR5). The effects of the TLR ligands on key cell functions and activation of signaling pathways were examined. The ability of PSCs to perform endocytosis and phagocytosis was also examined.

resultsPSCs expressed TLR2, 3, 4, and 5, as well as the associated molecules CD14 and MD2. All of the TLR ligands activated nuclear factor-kappaB, and three classes of mitogen-activated protein kinases (extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase). TLR ligands induced expression of monocyte chemoattractant protein 1, cytokine-induced neutrophil chemoattractant 1 (a rat homolog of interleukin-8), and inducible nitric oxide synthase, but not proliferation or type I collagen production. PSCs could perform fluid-phase and receptor-mediated endocytosis, as well as phagocytosis of Escherichia coli.

conclusionsPSCs expressed a variety of TLRs and responded to TLR ligands, leading to the activation of signaling pathways and proinflammatory responses. PSCs could process exogenous antigens by endocytosis and phagocytosis. PSCs might play a role in the immune functions of the pancreas through the recognition of PAMPs.

Indexed as

Gene ExpressionAnimalsBlotting, WesternCell ProliferationCells, CulturedChemokine CCL2Electrophoresis, Polyacrylamide GelImmunity, InnateLigandsLipopolysaccharide ReceptorsLymphocyte Antigen 96MaleMitogen-Activated Protein KinasesNF-kappa BNitric Oxide Synthase Type IIPancreasChemokine CCL2LigandsLipopolysaccharide ReceptorsLymphocyte Antigen 96Mitogen-Activated Protein KinasesNF-kappa BNitric Oxide Synthase Type IIRNATlr2 protein, ratTlr4 protein, ratToll-Like Receptor 2Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 5Toll-Like Receptors

Identifiers

PMID18592153
OpenAlexW2124158951

What OpenQuestion holds

Textmetadata
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.