Evidence map›Paper›PMID 19324975›Full record

ArticleAmerican journal of respiratory and critical care medicine2009

Protection from lipopolysaccharide-induced lung injury by augmentation of airway S-nitrosothiols.

Harvey E Marshall, Erin N Potts, Zachary T Kelleher, Jonathan S Stamler, W Michael Foster, Richard L Auten

RetractedErratum issued Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. It is linked to trial NCT03926741 (Methods to Identify and Treat Severe Asthma Patients Project 1), which is not on this map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 14% 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.

NCT03926741 early_phase1completednot on this mapstarted 2019, after this paper: background citation

Methods to Identify and Treat Severe Asthma Patients Project 1: GSNOR Phenotyping and GSNO Challenge

TypeinterventionalSponsorJames ReynoldsRan2019 to 2024Enrolled48ConditionsAsthmaArmsGSNO Challenge
3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. How to Define Early Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Budesonide inhalation ameliorates endotoxin-induced lung injury in rabbits.Experimental biology and medicine (Maywood, N.J.) · 2015
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. NOS2 regulation of LPS-induced airway inflammation via S-nitrosylation of NF-{kappa}B p65.American journal of physiology. Lung cellular and molecular physiology · 2011
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Harvey E MarshallDepartment of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA. marsh015@mc.duke.edu
Erin N Potts
Zachary T Kelleher
Jonathan S Stamler
W Michael Foster
Richard L Auten
Duke University · US

Funding

The Pathogenesis and Genetics of Environmental AsthmaU19ES012496 · NIEHS · DUKE UNIVERSITY · PI FOSTER, WILLIAM MICHAEL · 2004 to 2007
$6.4M
Research Core 3: Environmental Health PolicyP30ES011961 · NIEHS · DUKE UNIVERSITY · PI DI GIULIO, RICHARD · 2004 to 2009
$4.1M
S-nitrosothiols, NF-KappaB and Inflammation in Acute Lung InjuryR01HL092994 · NHLBI · DUKE UNIVERSITY · PI MARSHALL, HARVEY E · 2009 to 2017
$3.1M
NHLBI NIH HHS R01 HL092994NIEHS NIH HHS ES11961NIEHS NIH HHS U19-ES12496
6 · The paper itself

Abstract

rationaleS-Nitrosothiols (SNO) inhibit immune activation of the respiratory epithelium and airway SNO levels are decreased in inflammatory lung disease. Ethyl nitrite (ENO) is a gas with chemical properties favoring SNO formation. Augmentation of airway SNO by inhaled ENO treatment may decrease lung inflammation and subsequent injury by inhibiting activation of the airway epithelium.

objectivesTo determine the effect of inhaled ENO on airway SNO levels and LPS-induced lung inflammation/injury.

methodsMice were treated overnight with inhaled ENO (10 ppm) or air, followed immediately by exposure to aerosolized LPS or saline. Parameters of inflammation and lung injury were quantified 1 hour after completion of the aerosol exposure and correlated to lung airway and tissue SNO levels. MEASUREMENTS AND MAIN

resultsAerosolized LPS induced a decrease in airway and lung tissue SNO levels including S-nitrosylated NF-kappaB. The decrease in lung SNO was associated with an increase in lung NF-kappaB activity, cytokine/chemokine expression (keratinocyte-derived chemokine, tumor necrosis factor-alpha, and IL-6), airway neutrophil influx, and worsened lung compliance. Pretreatment with inhaled ENO restored airway SNO levels and reduced LPS-mediated NF-kappaB activation thereby inhibiting the downstream inflammatory response and preserving lung compliance.

conclusionsAirway SNO serves an antiinflammatory role in the lung. Inhaled ENO can be used to augment airway SNO and protect from LPS-induced acute lung injury.

Indexed as

Acute Lung InjuryAdministration, InhalationAnimalsAnti-Inflammatory AgentsMaleMiceNitritesS-NitrosothiolsAnti-Inflammatory Agentsethyl nitriteNitritesS-Nitrosothiols

Identifiers

PMID19324975
PMCPMC2701501
OpenAlexW2117858147

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.