Evidence map›Paper›PMID 37400850›Full record

ArticleParticle and fibre toxicology2023

Diesel Exhaust Particle (DEP)-induced glucose intolerance is driven by an intestinal innate immune response and NLRP3 activation in mice.

Angela J T Bosch, Theresa V Rohm, Shefaa AlAsfoor, Andy J Y Low, Zora Baumann, Neena Parayil, Faiza Noreen, Julien Roux, Daniel T Meier, Claudia Cavelti-Weder

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Particle and fibre toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Inhaled Pollutants of the Gero-Exposome and Later-Life Health.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
    Review
  6. Article
  7. Review
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

10 authors at 3 institutions in 2 countries.

Angela J T BoschDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Theresa V RohmDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Shefaa AlAsfoorDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Andy J Y LowDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Zora BaumannDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Neena ParayilDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Faiza NoreenDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Julien RouxDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Daniel T MeierDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland.
Claudia Cavelti-WederDepartment of Biomedicine, University of Basel, Basel, 4031, Switzerland. claudia.cavelti-weder@usz.ch.
University of Basel · CHSIB Swiss Institute of Bioinformatics · CHHospital Base · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe previously found that air pollution particles reaching the gastrointestinal tract elicit gut inflammation as shown by up-regulated gene expression of pro-inflammatory cytokines and monocyte/macrophage markers. This inflammatory response was associated with beta-cell dysfunction and glucose intolerance. So far, it remains unclear whether gut inflammatory changes upon oral air pollution exposure are causally linked to the development of diabetes. Hence, our aim was to assess the role of immune cells in mediating glucose intolerance instigated by orally administered air pollutants.

methodsTo assess immune-mediated mechanisms underlying air pollution-induced glucose intolerance, we administered diesel exhaust particles (DEP; NIST 1650b, 12 µg five days/week) or phosphate-buffered saline (PBS) via gavage for up to 10 months to wild-type mice and mice with genetic or pharmacological depletion of innate or adaptive immune cells. We performed unbiased RNA-sequencing of intestinal macrophages to elucidate signaling pathways that could be pharmacologically targeted and applied an in vitro approach to confirm these pathways.

resultsOral exposure to air pollution particles induced an interferon and inflammatory signature in colon macrophages together with a decrease of CCR2

conclusionIn mice, oral exposure to air pollution particles triggers an immune-mediated response in intestinal macrophages that contributes to the development of a diabetes-like phenotype. These findings point towards new pharmacologic targets in diabetes instigated by air pollution particles.

Indexed as

Glucose IntoleranceVehicle EmissionsAnimalsImmunity, InnateInflammationMiceNLR Family, Pyrin Domain-Containing 3 ProteinNLR Family, Pyrin Domain-Containing 3 ProteinVehicle EmissionsAir pollutionDiesel exhaust particlesGastrointestinal tractGlucose metabolismGut exposureIL-1βInnate immune responseMacrophagesMetabolic diseaseNLRP3

Identifiers

PMID37400850
PMCPMC10316612
OpenAlexW4382927857

What Socratic 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 Socratic graph.