Evidence map›Paper›PMID 26071220›Full record

ArticleInternational immunopharmacology2015

Keratinocyte nicotinic acetylcholine receptor activation modulates early TLR2-mediated wound healing responses.

Mari Kishibe, Tina M Griffin, Katherine A Radek

Open access · greenAbstract read
In one paragraph

Article in International immunopharmacology, 2015. 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
1.6field-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, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Ly6/uPAR Protein fromMarine drugs · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Topical nicotinic receptor activation improves wound bacterial infection outcomes and TLR2-mediated inflammation in diabetic mouse wounds.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2018
    Article
  14. Review
  15. Article
  16. Protective Effects ofIn vivo (Athens, Greece)
    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

3 authors at 1 institution in 1 country.

Mari KishibeThe Burn and Shock Trauma Research Institute, Loyola University Chicago, Health Science Division, Maywood, IL, USA; Department of Surgery, Loyola University Chicago, Health Science Division, Maywood, IL, USA. Electronic address: kradek1@luc.edu.
Tina M GriffinThe Burn and Shock Trauma Research Institute, Loyola University Chicago, Health Science Division, Maywood, IL, USA; Department of Surgery, Loyola University Chicago, Health Science Division, Maywood, IL, USA.
Katherine A RadekThe Burn and Shock Trauma Research Institute, Loyola University Chicago, Health Science Division, Maywood, IL, USA; Department of Surgery, Loyola University Chicago, Health Science Division, Maywood, IL, USA; Infectious Disease and Immunology Research Institute in the Department of Microbiology and Immunology, Loyola University Chicago, Health Science Division, Maywood, IL, USA; Stritch School of Medicine, Loyola University Chicago, Health Science Division, Maywood, IL, USA.
Loyola University Chicago · US

Funding

Linking Nicotinic Activation with Skin Innate Immunity and Atopic DermatitisR01AR061497 · NIAMS · LOYOLA UNIVERSITY CHICAGO · PI RADEK, KATHERINE AMANDA · 2012 to 2017
$2.0M
NIAMS NIH HHS R01 AR061497PHS HHS 1R01 ARO61497-01A1
6 · The paper itself

Abstract

The cholinergic anti-inflammatory pathway spans several macro- and micro-environments to control inflammation via α7 nicotinic acetylcholine receptors (nAChRs). Physiologic inflammation is necessary for normal wound repair and is triggered, in part, via Toll-like receptors (TLRs). Here, we demonstrate that keratinocyte nAChR activation dampens TLR2-mediated migration and pro-inflammatory cytokine and antimicrobial peptide (AMP) production, which is restored by a α7-selective nAChR antagonist. The mechanism of this response occurs by blocking the NF-κB and Erk1/2 pathway during early and late wound healing. In a mouse model of Staphylococcus aureus wound infection, topical nAChR activation reduces wound AMP and TLR2 production to augment bacterial survival in wild-type mice. These findings suggest that aberrant α7 nAChR activation may impair normal wound healing responses, and that pharmacologic administration of topical nAChR antagonists may improve wound healing outcomes in wounds necessitating a more robust inflammatory response.

Indexed as

AnimalsAntimicrobial Cationic PeptidesCathelicidinsCytokinesGene Expression RegulationHumansKeratinocytesMethicillin-Resistant Staphylococcus aureusMiceMice, Inbred C57BLNicotineReceptors, NicotinicSignal TransductionSkinStaphylococcal InfectionsToll-Like Receptor 2Antimicrobial Cationic PeptidesCathelicidinsCytokinesNicotineReceptors, NicotinicTlr2 protein, mouseToll-Like Receptor 2Antimicrobial peptidesInfectionKeratinocytesNicotinic receptorsToll-like receptor-2Wound healing

Identifiers

PMID26071220
PMCPMC4637223
OpenAlexW2184640338

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.