Evidence map›Paper›PMID 25997703›Full record

ArticleHuman cell2015

Photodynamic therapy mediates innate immune responses via fibroblast-macrophage interactions.

N Zulaziz, A Azhim, N Himeno, M Tanaka, Y Satoh, M Kinoshita, H Miyazaki, D Saitoh, N Shinomiya, Y Morimoto

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. 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

10 authors at 1 institution in 1 country.

N ZulazizDepartment of Electronic Systems Engineering, Malaysia-Japan International Institute of Technology, UTM, Kuala Lumpur, Malaysia.
A AzhimDepartment of Electronic Systems Engineering, Malaysia-Japan International Institute of Technology, UTM, Kuala Lumpur, Malaysia.
N HimenoiCAT Corporations, Osaka, Japan.
M TanakaJGSDF Kumamoto Hospital, Kumamoto, Japan.
Y SatohDepartment of Anesthesiology, National Defense Medical College, Tokorozawa, Japan.
M KinoshitaDepartment of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Japan.
H MiyazakiDivision of Traumatology, National Defense Medical College Research Institute, Tokorozawa, Japan.
D SaitohDivision of Traumatology, National Defense Medical College Research Institute, Tokorozawa, Japan.
N ShinomiyaDepartment of Integrated Physiology Bio-Nano Medicine, National Defense Medical College, Tokorozawa, Japan.
Y MorimotoDepartment of Integrated Physiology Bio-Nano Medicine, National Defense Medical College, Tokorozawa, Japan. moyan@ndmc.ac.jp.
National Defense Medical College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibacterial photodynamic therapy (PDT) has come to attract attention as an alternative therapy for drug-resistant bacteria. Recent reports revealed that antibacterial PDT induces innate immune response and stimulates abundant cytokine secretion as a part of inflammatory responses. However, the underlying mechanism how antibacterial PDT interacts with immune cells responsible for cytokine secretion has not been well outlined. In this study, we aimed to clarify the difference in gene expression and cytokine secretion between combined culture of fibroblasts and macrophages and their independent cultures. SCRC-1008, mouse fibroblast cell line and J774, mouse macrophage-like cell line were co-cultured and PDT treatments with different parameters were carried out. After various incubation periods (1-24 h), cells and culture medium were collected, and mRNA and protein levels for cytokines were measured using real-time PCR and ELISA, respectively. Our results showed that fibroblasts and macrophages interact with each other to mediate the immune response. We propose that fibroblasts initially respond to PDT by expressing Hspa1b, which regulates the NF-κB pathway via Tlr2 and Tlr4. Activation of the NF-κB pathway then results in an enhanced secretion of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) and neutrophil chemoattractant MIP-2 and KC from macrophages.

Indexed as

Immunity, InnatePhotochemotherapyCell MovementCells, CulturedChemokine CXCL1Chemokine CXCL2CytokinesFibroblastsHSP70 Heat-Shock ProteinsInflammation MediatorsInterleukin-1betaInterleukin-6MacrophagesNeutrophilsNF-kappa B p50 SubunitSignal TransductionChemokine CXCL1Chemokine CXCL2Cxcl1 protein, mouseCxcl2 protein, mouseCytokinesheat-shock protein 70.1HSP70 Heat-Shock ProteinsInflammation MediatorsInterleukin-1betaInterleukin-6NF-kappa B p50 SubunitNfkb1 protein, mouseTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alphaFibroblastImmune responseMacrophageNeutrophil migrationPDT

Identifiers

PMID25997703
OpenAlexW1897286730

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.