Evidence map›Paper›PMID 20061214›Full record

ArticleEnvironmental health perspectives2010

Particulate matter-induced airway hyperresponsiveness is lymphocyte dependent.

Vanessa Saunders, Patrick Breysse, Jennifer Clark, Alyssa Sproles, Melissa Davila, Marsha Wills-Karp

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2010. 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
4.7field-weighted citation impact, top 5% 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, 62 citations in OpenAlex.

  1. Article
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  9. Review
  10. Exposure to NOClinical epigenetics · 2018
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  11. Breaking Steroid Resistance: Effect of Vitamin D on IL-23.American journal of respiratory cell and molecular biology · 2017
    Article
  12. Vitamin D Counteracts an IL-23-Dependent IL-17AAmerican journal of respiratory cell and molecular biology · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Proximity to a Major Road and Plasma Cytokines in School-Aged Children.Pediatric allergy, immunology, and pulmonology · 2016
    Article
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Vanessa SaundersDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229 , USA.
Patrick Breysse
Jennifer Clark
Alyssa Sproles
Melissa Davila
Marsha Wills-Karp
Cincinnati Children's Hospital Medical Center · USJohns Hopkins University · US

Funding

Oxidative Stress & Inflammation in a Human PM Nasal ChallengeP50ES015903 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI BREYSSE, PATRICK N · 2007 to 2011
$12.1M
Trial of Behavioral Changes in Home Exposure ControlP01ES009606 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI DIETTE, GREGORY B · 1999 to 2008
$6.8M
NIEHS NIH HHS P01 ES009606NIEHS NIH HHS P01ES009606NIEHS NIH HHS P50 ES015903
6 · The paper itself

Abstract

backgroundExposure to airborne particulate matter (PM), a major component of air pollution, has been associated with increases in both exacerbations of and hospitalizations for asthma. We have previously shown that exposure to ambient PM collected in urban Baltimore (AUB) induces airway hyperresponsiveness (AHR), eosinophilic and neutrophilic inflammation, and the recruitment of T cells. However, the mechanism(s) by which it induces these features of asthma remains unknown.

objectiveWe investigated whether T lymphocytes play a role in AUB-induced AHR.

methodsWe compared the effects of AUB exposure on the allergic phenotype in wild-type (WT) BALB/c mice and in mice deficient in recombinase-activating gene-1 (Rag1-/-) that lack mature lymphocytes.

resultsWe found that exposure of WT mice to AUB induced AHR concomitant with increases in the numbers of bronchoalveolar lavage (BAL) fluid lymphocytes, eosinophils, neutrophils, and mucus-containing cells in the lungs of WT mice. Interestingly, we show for the first time that these effects were associated with significant elevations in interleukin (IL)-17A, IL-17F, and T-helper 2 cell (TH2) (IL-13, IL-5) cytokine levels in lung cells, as well as reductions in the levels of the suppressive cytokine IL-10. Interestingly, Rag1-/- mice failed to develop AUB-induced AHR; however, AUB-induced BAL fluid cellularity, and mucus cell changes were only partially inhibited in Rag1-/- mice.

conclusionsTaken together, our results suggest that AUB exposure increases the pathophysiological features of asthma via activation of lymphocyte-dependent pathways. These results provide a plausible biological mechanism for the strong association between PM exposure and the increased severity of asthma.

Indexed as

Air PollutantsAnimalsAsthmaBaltimoreBronchial HyperreactivityBronchoalveolar Lavage FluidCytokinesFemaleHomeodomain ProteinsHumansImmunoglobulin ELungMaleMiceMice, Inbred BALB CMice, KnockoutAir PollutantsCytokinesHomeodomain ProteinsImmunoglobulin EParticulate MatterRAG-1 protein

Identifiers

PMID20061214
PMCPMC2866679
OpenAlexW2050882700

What OpenQuestion holds

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LicenceCC0
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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.