Evidence map›Paper›PMID 29047037›Full record

ReviewInflammation2018

Diesel Exhaust Particles and the Induction of Macrophage Activation and Dysfunction.

Akeem O Lawal

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Assessing Causality Between Second-Hand Smoking and Potentially Associated Diseases in Multiple Systems: A Two-Sample Mendelian Randomization Study.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2024
    Article
  9. Review
  10. Article
  11. Review
  12. Micro- and Nanosized Substances Cause Different Autophagy-Related Responses.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

1 author.

Akeem O LawalMolecular Biology and Bioinformatic Unit, Department of Biochemistry, School of Sciences, Federal University of Technology, Akure P.M.B. 704, Akure, Ondo State, Nigeria. tolekan@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diesel exhaust particles (DEP) are an important component of air particulate matter, generated from the incomplete combustion of fossil fuel in diesel engines. Several epidemiological and experimental data have shown the ability of DEP to induce oxidative stress and pro-inflammatory response as mechanisms in macrophage activation and dysfunction. Macrophages are very important to immunity and immune response due to their ability to phagocyte microbes and parasites. They also respond to toxic chemicals, such as DEP, in the environment and studies have shown that their functions may be impaired by their exposure to DEP. For instance, the ultrafine particles (UFP) of DEP are capable of penetrating deep into the lungs and getting deposited in the alveolar component, where they can mitigate against the phagocytosis function of the alveolar macrophages. In this review, data linking DEP exposure to macrophage activation and dysfunction are addressed together with the various mechanisms involved in these DEP-induced effects.

Indexed as

AnimalsHumansInflammation MediatorsInhalation ExposureMacrophage ActivationMacrophages, AlveolarOxidative StressParticulate MatterPhagocytosisVehicle EmissionsInflammation MediatorsParticulate MatterVehicle Emissionsair particulate matterdiesel exhaust particlesmacrophagesoxidative stresspro-inflammatory effects

Identifiers

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.