Evidence map›Paper›PMID 29678746›Full record

ArticleThe Journal of allergy and clinical immunology2018

Thirdhand smoke component can exacerbate a mouse asthma model through mast cells.

Mang Yu, Kaori Mukai, Mindy Tsai, Stephen J Galli

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of allergy and clinical immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The External Exposome and Food Allergy.Current allergy and asthma reports · 2020
    Review
  8. Article
  9. Review
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Mang YuDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif; Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, Calif. Electronic address: yumyu@staford.edu.
Kaori MukaiDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif; Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, Calif.
Mindy TsaiDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif; Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, Calif.
Stephen J GalliDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif; Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, Calif; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, Calif. Electronic address: sgalli@stanford.edu.
Stanford University · US

Funding

Expression and Modulation of Mast Cell Function in AsthmaR01AI070813 · NIAID · STANFORD UNIVERSITY · PI GALLI, STEPHEN JOSEPH · 2006 to 2010
$2.5M
RabGEF1 in MyD88 signaling, skin immunity, and atopic dermatitisR01AR067145 · NIAMS · STANFORD UNIVERSITY · PI GALLI, STEPHEN JOSEPH · 2015 to 2019
$1.9M
NIAID NIH HHS R01 AI070813NIAMS NIH HHS R01 AR067145
6 · The paper itself

Abstract

backgroundThirdhand smoke (THS) represents the accumulation of secondhand smoke on indoor surfaces and in dust, which, over time, can become more toxic than secondhand smoke. Although it is well known that children of smokers are at increased risk for asthma or asthma exacerbation if the disease is already present, how exposure to THS can influence the development or exacerbation of asthma remains unknown.

objectiveWe investigated whether epicutaneous exposure to an important component of THS, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), can influence asthma pathology in a mouse model elicited by means of repeated intranasal challenge with cockroach antigen (CRA).

methodsWild-type mice, α7 nicotinic acetylcholine receptor (nAChR)- or mast cell (MC)-deficient mice, and mice with MCs that lacked α7 nAChRs or were the host's sole source of α7 nAChRs were subjected to epicutaneous NNK exposure, intranasal CRA challenge, or both, and the severity of features of asthma pathology, including airway hyperreactivity, airway inflammation, and airway remodeling, was assessed.

resultsWe found that α7 nAChRs were required to observe adverse effects of epicutaneous NNK exposure on multiple features of CRA-induced asthma pathology. Moreover, MC expression of α7 nAChRs contributed significantly to the ability of epicutaneous NNK exposure to exacerbate airway hyperreactivity to methacholine, airway inflammation, and airway remodeling in this model.

conclusionOur results show that skin exposure to NNK, a component of THS, can exacerbate multiple features of a CRA-induced model of asthma in mice and define MCs as key contributors to these adverse effects of NNK.

Indexed as

Tobacco Smoke PollutionAdministration, IntranasalAllergensalpha7 Nicotinic Acetylcholine ReceptorAnimalsAsthmaCockroachesCytokinesDisease Models, AnimalFemaleLungMast CellsMice, Inbred C57BLMice, TransgenicNitrosaminesOvalbumin4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanoneAllergensalpha7 Nicotinic Acetylcholine ReceptorCytokinesNitrosaminesOvalbuminSmokeTobacco Smoke Pollution4-(methylnitrosamino)-1-(3-pyridyl)-1-butanonecockroach allergenmast cellsThirdhand smokeα7 nicotinic acetylcholine receptor

Identifiers

PMID29678746
PMCPMC6193858
OpenAlexW2801296114

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.