Evidence map›Paper›PMID 33665636›Full record

ArticleBrain, behavior, & immunity - health2020

Dopamine activates NF-κB and primes the NLRP3 inflammasome in primary human macrophages.

R A Nolan, K L Reeb, Y Rong, S M Matt, H S Johnson, K Runner, P J Gaskill

Open access · hybridAbstract read
In one paragraph

Article in Brain, behavior, & immunity - health, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

37 citing papers in PubMed, 45 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

R A NolanDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102.
K L ReebDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102.
Y RongDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102.
S M MattDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102.
H S JohnsonDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102.
K RunnerDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102.
P J GaskillDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102.
Drexel University · US

Funding

Mechanisms of dopamine mediated increase in HIV infection of macrophagesR01DA039005 · NIDA · DREXEL UNIVERSITY · PI GASKILL, PETER JESSE · 2015 to 2019
$1.9M
NIDA NIH HHS R01 DA039005
6 · The paper itself

Abstract

Induction of innate immune genes in the brain is thought to be a major factor in the development of addiction to substances of abuse. As the major component of the innate immune system in the brain, aberrant activation of myeloid cells such as macrophages and microglia due to substance use may mediate neuroinflammation and contribute to the development of addiction. All addictive drugs modulate the dopaminergic system and our previous studies have identified dopamine as a pro-inflammatory modulator of macrophage function. However, the mechanism that mediates this effect is currently unknown. Inflammatory activation of macrophages and induction of cytokine production is often mediated by the transcription factor NF-κB, and prior studies have shown that dopamine can modulate NF-κB activity in T-cells and other non-immune cell lines. Here we demonstrated that dopamine can activate NF-κB in primary human macrophages, resulting in the induction of its downstream targets including the NLRP3 inflammasome and the inflammatory cytokine IL-1β. These data also indicate that dopamine primes but does not activate the NLRP3 inflammasome in human macrophages. Activation of NF-κB was required for dopamine-mediated increases in IL-1β, as an inhibitor of NF-κB was able to abrogate the effects of dopamine on production of these cytokines. Connecting an increase in extracellular dopamine to NF-κB activation and inflammation suggests specific intracellular targets that could be used to ameliorate the inflammatory impact of dopamine in neuroinflammatory conditions associated with myeloid cell activation such as addiction.

Indexed as

Dopaminedrug abusemacrophagesneuroinflammationNF-κBNLRP3

Identifiers

PMID33665636
PMCPMC7929492
OpenAlexW2997275869

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.