Evidence map›Paper›PMID 30073204›Full record

ArticleBiochemistry and biophysics reports2018

The anti-inflammatory effect of LMWF5A and N-acetyl kynurenine on macrophages: Involvement of aryl hydrocarbon receptor in mechanism of action.

Leonard T Rael, Raphael Bar-Or, Kaysie L Banton, Charles W Mains, Michael Roshon, Allen H Tanner, Mark J Lieser, David L Acuna, David Bar-Or

Abstract read
In one paragraph

Article in Biochemistry and biophysics reports, 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Multiomics Analysis Reveals the Impact of Microbiota on Host Metabolism in Hepatic Steatosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. 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

9 authors.

Leonard T RaelSwedish Medical Center, Englewood, CO 80113, USA.
Raphael Bar-OrSwedish Medical Center, Englewood, CO 80113, USA.
Kaysie L BantonSwedish Medical Center, Englewood, CO 80113, USA.
Charles W MainsSt. Anthony Hospital, Lakewood, CO 80228, USA.
Michael RoshonPenrose Hospital, Colorado Springs, CO 80907, USA.
Allen H TannerPenrose Hospital, Colorado Springs, CO 80907, USA.
Mark J LieserResearch Medical Center, Kansas City, MO 64132, USA.
David L AcunaWesley Medical Center, Wichita, KS 67214, USA.
David Bar-OrSwedish Medical Center, Englewood, CO 80113, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After a traumatic insult, macrophages can become activated leading to general inflammation at the site of injury. Activated macrophages are partially regulated by the aryl hydrocarbon receptor (AhR) which when activated suppresses inflammation by limiting the secretion of pro-inflammatory cytokines and promoting the over expression of immuno-modulatory mediators. This study aims to determine whether the low molecular weight fraction of 5% human serum albumin (LMWF5A) and N-acetyl kynurenine (NAK), an N-acetyl tryptophan (NAT) breakdown product in LMWF5A, can regulate inflammation by inhibiting macrophage activation through the AhR since kynurenine is a known AhR agonist. Using LCMS, we demonstrate that NAT is non-enzymatically degraded during accelerated aging of LMWF5A with high heat accelerating degradation. More importantly, NAK is a major degradation product found in LMWF5A. THP-1 monocytes were differentiated into macrophages using phorbol 12-myristate 13-acetate (PMA) and pre-treated with 2-fold dilutions of LMWF5A or synthetic NAK with or without an AhR antagonist (CH223191) prior to overnight stimulation with lipopolysaccharide (LPS). Treatment with LMWF5A caused a 50-70% decrease in IL-6 release throughout the dilution series. A dose-response inhibition of IL-6 release was observed for NAK with maximal inhibition (50%) seen at the highest NAK concentration. Finally, an AhR antagonist partially blocked the anti-inflammatory effect of LMWF5A while completely blocking the effect of NAK. A similar inhibitory effect was observed for CXCL-10, but the AhR antagonist was not effective suggesting additional mechanisms for CXCL-10 release. These preliminary findings suggest that LMWF5A and NAK partially promote the suppression of activated macrophages via the AhR receptor. Therefore, LMWF5A, which contains NAK, is potentially a useful therapeutic in medical conditions where inflammation is prevalent such as trauma, sepsis, and wound healing.

Indexed as

AhR, aryl hydrocarbon receptorAryl hydrocarbon receptorESI+, electrospray positive ionizationHSA, human serum albuminHuman serum albuminInflammationKYN, kynurenineKynurenineLCMS, liquid chromatography-mass spectrometryLMWF5A, low molecular weight fraction of 5% albuminMacrophagesNAK, N-acetyl kynurenineNAT, N-acetyl tryptophanTryptophan

Identifiers

PMID30073204
PMCPMC6068081

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.