ArticlePloS one2012
Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Who cites it
16 citing papers in PubMed, 53 citations in OpenAlex.
- Inflammation induced by inhaled lipopolysaccharide depends on particle size in healthy volunteers.British journal of clinical pharmacology · 2016Trial
- Dissociation between systemic and pulmonary anti-inflammatory effects of dexamethasone in humans.British journal of clinical pharmacology · 2016Trial
- Rewiring the Lung-CNS Axis After Spinal Cord Injury.Journal of inflammation research · 2026Review
- Anti-atherosclerotic effects and molecular targets of salvianolic acids fromFrontiers in pharmacology · 2025Review
- Targeting transitioning lung monocytes/macrophages as treatment strategies in lung disease related to environmental exposures.Respiratory research · 2024Article
- Aconitate decarboxylase 1 mediates the acute airway inflammatory response to environmental exposures.Frontiers in immunology · 2024Article
- Characterization of the lung microbiome and inflammatory cytokine levels in women exposed to environmental risk factors: A pilot study.Immunity, inflammation and disease · 2023Article
- Association of exacerbation phenotype with the sputum microbiome in chronic obstructive pulmonary disease patients during the clinically stable state.Journal of translational medicine · 2021Article
- Prediction of survival of diffuse large B-cell lymphoma patients via the expression of three inflammatory genes.Cancer medicine · 2016Article
- Holi colours contain PM10 and can induce pro-inflammatory responses.Journal of occupational medicine and toxicology (London, England) · 2016Article
- Alpha-Tomatine Exhibits Anti-inflammatory Activity in Lipopolysaccharide-Activated Macrophages.Inflammation · 2015Article
- Article
- Effect of inhaled endotoxin on mucociliary clearance and airway inflammation in mild smokers and nonsmokers.Journal of aerosol medicine and pulmonary drug delivery · 2014Article
- Advances in device and formulation technologies for pulmonary drug delivery.AAPS PharmSciTech · 2014Review
- Airway hyper-responsiveness in lipopolysaccharide-challenged common marmosets (Callithrix jacchus).Clinical science (London, England : 1979) · 2014Article
- The stimulated innate resistance event in Bordetella pertussis infection is dependent on reactive oxygen species production.Infection and immunity · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endotoxin (Lipopolysaccharide, LPS) is a potent inducer of inflammation and there is various LPS contamination in the environment, being a trigger of lung diseases and exacerbation. The objective of this study was to assess the time course of inflammation and the sensitivities of the airways and alveoli to targeted LPS inhalation in order to understand the role of LPS challenge in airway disease.In healthy volunteers without any bronchial hyperresponsiveness we targeted sequentially 1, 5 and 20 µg LPS to the airways and 5 µg LPS to the alveoli using controlled aerosol bolus inhalation. Inflammatory parameters were assessed during a 72 h time period. LPS deposited in the airways induced dose dependent systemic responses with increases of blood neutrophils (peaking at 6 h), Interleukin-6 (peaking at 6 h), body temperature (peaking at 12 h), and CRP (peaking at 24 h). 5 µg LPS targeted to the alveoli caused significantly stronger effects compared to 5 µg airway LPS deposition. Local responses were studied by measuring lung function (FEV(1)) and reactive oxygen production, assessed by hydrogen peroxide (H(2)O(2)) in fractionated exhaled breath condensate (EBC). FEV(1) showed a dose dependent decline, with lowest values at 12 h post LPS challenge. There was a significant 2-fold H(2)O(2) induction in airway-EBC at 2 h post LPS inhalation. Alveolar LPS targeting resulted in the induction of very low levels of EBC-H(2)O(2).Targeting LPS to the alveoli leads to stronger systemic responses compared to airway LPS targeting. Targeted LPS inhalation may provide a novel model of airway inflammation for studying the role of LPS contamination of air pollution in lung diseases, exacerbation and anti-inflammatory drugs.
Indexed as
Identifiers
What OpenQuestion holds
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.