Evidence map›Paper›PMID 17023730›Full record

Trial reportAmerican journal of respiratory and critical care medicine2006

Glutathione s-transferases M1 and P1 prevent aggravation of allergic responses by secondhand smoke.

Frank D Gilliland, Yu-Fen Li, Henry Gong, David Diaz-Sanchez

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in American journal of respiratory and critical care medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Article
  8. Air pollutants and early origins of respiratory diseases.Chronic diseases and translational medicine · 2018
    Article
  9. Article
  10. Review
  11. Allergic diseases and air pollution.Asia Pacific allergy · 2013
    Article
  12. Article
  13. Glutathione S-transferase P1 Ile105Val polymorphism modulates allergen-induced airway inflammation in human atopic asthmatics in vivo.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2013
    Article
  14. Article
  15. Role of GSTM1 in resistance to lung inflammation.Free radical biology & medicine · 2012
    Review
  16. Article
  17. The effect of environmental oxidative stress on airway inflammation.Current opinion in allergy and clinical immunology · 2012
    Review
  18. Review
  19. Unravelling gene-by-environment effects in asthma and allergy: the glutathione pathway as an early success story.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2011
    Article
  20. Oxidative stress in asthma.The World Allergy Organization journal · 2011
    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

4 authors at 1 institution in 2 countries.

Frank D GillilandDepartment of Preventive Medicine, Keck School of Medicine, University of Southern California, 1540 Alcazar Street, CHP 236, Los Angeles, CA 90033, USA. gillilan@usc.edu
Yu-Fen Li
Henry Gong
David Diaz-Sanchez
University of Southern California · US

Funding

Translational Research Support CoreP30ES007048 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Joseph Leo Wiemels · 1996 to 2026
$46.4M
Urban Air Pollution and Children's Respiratory HealthP01ES011627 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AVOL, EDWARD · 2002 to 2011
$30.2M
Xenobiotics and Allergic InflammationP01AI050495 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAXON, ANDREW · 2001 to 2005
$7.1M
Urban Air Pollution &Persistent Early Life AsthmaP01ES009581 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GILLILAND, FRANK D. · 1999 to 2010
$6.8M
FACTORS IN CHILDHOOD LUNG SUSCEPTIBILITY TO POLLUTIONR01HL061768 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GILLILAND, FRANK D. · 1999 to 2008
$4.4M
Air Pollution, Inflammation and New Onset AsthmaR01HL076647 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GILLILAND, FRANK D. · 2005 to 2009
$3.6M
NHLBI NIH HHS 5R01HL076647NHLBI NIH HHS 5R01HL61768NIAID NIH HHS 5P01AI050495NIEHS NIH HHS 5P01ES009581NIEHS NIH HHS 5P01ES011627NIEHS NIH HHS 5P30ES007048
6 · The paper itself

Abstract

rationaleSecondhand tobacco smoke (SHS) and traffic-related air pollutants are associated with asthma and allergy. Diesel exhaust particles (DEPs) and SHS can interact with allergens in exacerbating allergic airway diseases through generation of reactive oxygen species. Glutathione S-transferases (GSTs) metabolize reactive oxygen species and detoxify electrophilic xenobiotics present in SHS and DEPs.

objectivesWe tested the hypotheses that functional GSTM1-null genotype and GSTP1 codon 105 variants (Ile105 and Val105) are determinants of allergic responses to SHS, and that responses to SHS and DEPs are correlated. METHODS AND MEASUREMENTS: In a randomized, placebo-controlled crossover trial, 19 ragweed allergen-sensitive subjects who had previously participated in a DEP trial were challenged intranasally with allergen after having been exposed to either clean air or SHS at separate visits. Nasal allergen-specific IgE, histamine, IL-4, and IFN-gamma levels were measured before and after allergen challenge. MAIN

resultsIndividuals with GSTM1-null or GSTP1 Ile105 genotypes showed larger nasal responses to allergens with SHS compared with clean air. GSTM1-null subjects had a larger increase in IgE than GSTM1-present subjects (median, 173.3 vs. 46.7 U/ml; p = 0.03), and the Ile105 GSTP1 genotype subjects had increased histamine (median, 10.2 vs. 4.6 nM; p = 0.01) after SHS plus allergen challenge. Responses to SHS and DEPs were correlated. Enhancement of IgE and histamine was greatest in the subjects with both the GSTM1-null and GSTP1 Ile/Ile genotypes.

conclusionsGSTM1 and GSTP1 are important cytoprotective factors that reduce SHS and DEP exacerbation of allergic responses.

Indexed as

AdultAllergensCross-Over StudiesFemaleGenotypeGlutathione S-Transferase piGlutathione TransferaseHistamineHumansImmunoglobulin EInterferon-gammaInterleukin-4MaleMiddle AgedRespiratory HypersensitivityTobacco Smoke PollutionAllergensGlutathione S-Transferase piGlutathione TransferaseGSTP1 protein, humanHistamineImmunoglobulin EInterferon-gammaInterleukin-4Tobacco Smoke PollutionVehicle Emissions

Identifiers

PMID17023730
PMCPMC2648296
OpenAlexW1993444320

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.