Evidence map›Paper›PMID 30567499›Full record

ArticleBMC immunology2018

5-Aminolevulinic acid regulates the immune response in LPS-stimulated RAW 264.7 macrophages.

Yuta Sugiyama, Yukari Hiraiwa, Yuichiro Hagiya, Motowo Nakajima, Tohru Tanaka, Shun-Ichiro Ogura

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2018. 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
1.7field-weighted citation impact, top 15% 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, 38 citations in OpenAlex.

  1. Trial
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  8. Understanding immune-modulatory efficacy in vitro.Chemico-biological interactions · 2022
    Review
  9. Article
  10. Article
  11. Crosstalk between Metabolic Disorders and Immune Cells.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Anti-Inflammatory and Antioxidant Effects ofMediators of inflammation · 2020
    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 2 institutions in 1 country.

Yuta SugiyamaSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Kanagawa, Japan.
Yukari HiraiwaSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Kanagawa, Japan.
Yuichiro HagiyaSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Kanagawa, Japan.
Motowo NakajimaSBI Pharma CO., LTD., Roppongi, Tokyo, 106-6020, Japan.
Tohru TanakaSBI Pharma CO., LTD., Roppongi, Tokyo, 106-6020, Japan.
Shun-Ichiro OguraSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Kanagawa, Japan. sogura@bio.titech.ac.jp.ORCID 0000-0002-4673-8882
Tokyo Institute of Technology · JPSBI Pharmaceuticals (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMacrophages are crucial players in a variety of inflammatory responses to environmental cues. However, it has been widely reported that macrophages cause chronic inflammation and are involved in a variety of diseases, such as obesity, diabetes, metabolic syndrome, and cancer. In this study, we report the suppressive effect of 5-aminolevulinic acid (ALA), via the HO-1-related system, on the immune response of the LPS-stimulated mouse macrophage cell line RAW264.7.

resultsRAW264.7 cells were treated with LPS with or without ALA, and proinflammatory mediator expression levels and phagocytic ability were assessed. ALA treatment resulted in the attenuation of iNOS and NO expression and the downregulation of proinflammatory cytokines (TNF-α, cyclooxygenase2, IL-1β, IL-6). In addition, ALA treatment did not affect the phagocytic ability of macrophages. To our knowledge, this study is the first to investigate the effect of ALA on macrophage function. Our findings suggest that ALA may have high potential as a novel anti-inflammatory agent.

conclusionsIn the present study, we showed that exogenous addition of ALA induces HO-1 and leads to the downregulation of NO and some proinflammatory cytokines. These findings support ALA as a promising anti-inflammatory agent.

Indexed as

Aminolevulinic AcidAnimalsAnti-Inflammatory Agents, Non-SteroidalCytokinesHeme Oxygenase-1Levulinic AcidsLipopolysaccharidesMacrophagesMiceNitric OxideRAW 264.7 CellsAminolevulinic AcidAnti-Inflammatory Agents, Non-SteroidalCytokinesHeme Oxygenase-1Levulinic AcidsLipopolysaccharidesNitric Oxide5-Aminolevulinic acidAnti inflammationHeme oxygenase-1LPSMacrophage

Identifiers

PMID30567499
PMCPMC6300011
OpenAlexW2903694927

What OpenQuestion holds

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LicenceCC BY
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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.