Evidence map›Paper›PMID 18250191›Full record

ArticleThe Journal of experimental medicine2008

Ozone exposure in a mouse model induces airway hyperreactivity that requires the presence of natural killer T cells and IL-17.

Muriel Pichavant, Sho Goya, Everett H Meyer, Richard A Johnston, Hye Y Kim, Ponpan Matangkasombut, Ming Zhu, Yoichiro Iwakura, Paul B Savage, Rosemarie H DeKruyff and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed
26.2field-weighted citation impact, top 1% 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

151 citing papers in PubMed, 303 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Article
  7. Article
  8. Interleukin-11 receptor subunit α-1 is required for maximal airway responsiveness to methacholine after acute exposure to ozone.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Review
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  14. Innate-like Lymphocytes and Innate Lymphoid Cells in Asthma.Clinical reviews in allergy & immunology · 2020
    Review
  15. Review
  16. Article
  17. Review
  18. TRPC6-dependent CaCell death & disease · 2020
    Article
  19. Review
  20. Review

91 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

12 authors at 4 institutions in 2 countries.

Muriel PichavantChildren's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA.
Sho Goya
Everett H Meyer
Richard A Johnston
Hye Y Kim
Ponpan Matangkasombut
Ming Zhu
Yoichiro Iwakura
Paul B Savage
Rosemarie H DeKruyff
Stephanie A Shore
Dale T Umetsu
Boston Children's Hospital · USMassachusetts Department of Public Health · USBrigham Young University · USThe University of Tokyo · JP

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
TIM recognition of phosphatidylserine regulates innate and adaptive immunityP01AI054456 · NIAID · STANFORD UNIVERSITY · PI FREEMAN, GORDON JAMES · 2003 to 2014
$12.8M
THE ROLE OF TH CELL SUBSETS AND ALLERGIC LUNG INFLAMMATIR01HL062348 · NHLBI · STANFORD UNIVERSITY · PI UMETSU, DALE T · 1999 to 2007
$2.6M
NHLBI NIH HHS HL062348NHLBI NIH HHS R01 HL062348NIAID NIH HHS AI054456NIAID NIH HHS P01 AI054456NIAID NIH HHS T32 AI007290
6 · The paper itself

Abstract

Exposure to ozone, which is a major component of air pollution, induces a form of asthma that occurs in the absence of adaptive immunity. Although ozone-induced asthma is characterized by airway neutrophilia, and not eosinophilia, it is nevertheless associated with airway hyperreactivity (AHR), which is a cardinal feature of asthma. Because AHR induced by allergens requires the presence of natural killer T (NKT) cells, we asked whether ozone-induced AHR had similar requirements. We found that repeated exposure of wild-type (WT) mice to ozone induced severe AHR associated with an increase in airway NKT cells, neutrophils, and macrophages. Surprisingly, NKT cell-deficient (CD1d(-/-) and Jalpha18(-/-)) mice failed to develop ozone-induced AHR. Further, treatment of WT mice with an anti-CD1d mAb blocked NKT cell activation and prevented ozone-induced AHR. Moreover, ozone-induced, but not allergen-induced, AHR was associated with NKT cells producing interleukin (IL)-17, and failed to occur in IL-17(-/-) mice nor in WT mice treated with anti-IL-17 mAb. Thus, ozone exposure induces AHR that requires the presence of NKT cells and IL-17 production. Because NKT cells are required for the development of two very disparate forms of AHR (ozone- and allergen-induced), our results strongly suggest that NKT cells mediate a unifying pathogenic mechanism for several distinct forms of asthma, and represent a unique target for effective asthma therapy.

Indexed as

Air PollutantsAnimalsBronchial HyperreactivityBronchoalveolar Lavage FluidDisease Models, AnimalInterleukin-13Interleukin-17Interleukin-4Killer Cells, NaturalLeukocyte CountMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutOvalbuminOzoneAir PollutantsInterleukin-13Interleukin-17Interleukin-4OvalbuminOzone

Identifiers

PMID18250191
PMCPMC2271004
OpenAlexW2166428721

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.