Evidence map›Paper›PMID 19645497›Full record

ArticleChemical research in toxicology2009

Macrophages and inflammatory mediators in chemical toxicity: a battle of forces.

Debra L Laskin

Open access · greenAbstract read
In one paragraph

Article in Chemical research in toxicology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

148 citing papers in PubMed, 282 citations in OpenAlex.

  1. Review
  2. Engineering Oncolytic Virus-Armed Macrophages for Enhanced Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Review
  4. Article
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  8. Phytochemical Analysis and Phytometabolomic Profiling ofInternational journal of molecular sciences · 2025
    Article
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  10. Review
  11. Article
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  14. Review
  15. Review
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  17. Promising roles ofJournal of agriculture and food research · 2023
    Article
  18. Review
  19. Article
  20. Review

88 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Debra L LaskinDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, New Jersey 08854.
Rutgers, The State University of New Jersey · US

Funding

UMDNJ/Rutgers University CounterACT Research Center of ExcellenceU54AR055073 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HECK, DIANE E · 2006 to 2024
$71.4M
Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ROBERT John LAUMBACH · 1988 to 2026
$47.4M
ACTIVATED MACROPHAGES AND OZONE TOXICITYR01ES004738 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI Debra L Laskin · 1989 to 2026
$9.0M
ROLE OF KUPFFER CELLS IN CHEMICAL TOXICITYR01GM034310 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI LASKIN, DEBRA L · 1985 to 2009
$3.1M
Macrophages and Inflammatory Mediators in Silica-Induced CarcinogenesisR01CA132624 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI LASKIN, DEBRA L · 2008 to 2012
$1.5M
NCI NIH HHS CA132624NCI NIH HHS R01 CA132624NIAMS NIH HHS AR055073NIAMS NIH HHS U54 AR055073NIEHS NIH HHS ES004738NIEHS NIH HHS ES005022NIEHS NIH HHS P30 ES005022NIEHS NIH HHS R01 ES004738NIGMS NIH HHS GM034310NIGMS NIH HHS R01 GM034310
6 · The paper itself

Abstract

Macrophages function as control switches of the immune system, providing a balance between pro- and anti-inflammatory responses. To accomplish this, they develop into different subsets: classically (M1) or alternatively (M2) activated macrophages. Whereas M1 macrophages display a cytotoxic, proinflammatory phenotype, much like the soldiers of The Dark Side of The Force in the Star Wars movies, M2 macrophages, like Jedi fighters, suppress immune and inflammatory responses and participate in wound repair and angiogenesis. Critical to the actions of these divergent or polarized macrophage subpopulations is the regulated release of inflammatory mediators. When properly controlled, M1 macrophages effectively destroy invading pathogens, tumor cells, and foreign materials. However, when M1 activation becomes excessive or uncontrolled, these cells can succumb to The Dark Side, releasing copious amounts of cytotoxic mediators that contribute to disease pathogenesis. The activity of M1 macrophages is countered by The Force of alternatively activated M2 macrophages, which release anti-inflammatory cytokines, growth factors, and mediators involved in extracellular matrix turnover and tissue repair. It is the balance in the production of mediators by these two macrophage subpopulations that ultimately determines the outcome of the tissue response to chemical toxicants.

Indexed as

AnimalsAnti-Inflammatory AgentsCell Culture TechniquesCell ProliferationCells, CulturedCell SurvivalCytokinesHumansImmune SystemImmunity, InnateInflammation MediatorsLeukocytes, MononuclearMacrophagesMiceMice, Inbred C57BLSpinal Cord InjuriesAnti-Inflammatory AgentsCytokinesInflammation Mediators

Identifiers

PMID19645497
PMCPMC2787782
OpenAlexW2053891616

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.