Evidence map›Paper›PMID 38242945›Full record

ArticleScientific reports2024

Transcriptomic characterization of the human segmental endotoxin challenge model.

Christina Gress, Tobias Litzenburger, Ramona Schmid, Ke Xiao, Florian Heissig, Meike Muller, Abhya Gupta, Jens M Hohlfeld

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 3 institutions in 1 country.

Christina GressFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Clinical Airway Research, 30625, Hannover, Germany.
Tobias LitzenburgerBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Ramona SchmidBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Ke XiaoFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Clinical Airway Research, 30625, Hannover, Germany.
Florian HeissigBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Meike MullerFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Clinical Airway Research, 30625, Hannover, Germany.
Abhya GuptaBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Jens M HohlfeldFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Clinical Airway Research, 30625, Hannover, Germany. jens.hohlfeld@item.fraunhofer.de.ORCID 0000-0003-2646-6186
Boehringer Ingelheim (Germany) · DEFraunhofer Institute for Toxicology and Experimental Medicine · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Segmental instillation of lipopolysaccharide (LPS) by bronchoscopy safely induces transient airway inflammation in human lungs. This model enables investigation of pulmonary inflammatory mechanisms as well as pharmacodynamic analysis of investigational drugs. The aim of this work was to describe the transcriptomic profile of human segmental LPS challenge with contextualization to major respiratory diseases. Pre-challenge bronchoalveolar lavage (BAL) fluid and biopsies were sampled from 28 smoking, healthy participants, followed by segmental instillation of LPS and saline as control. Twenty-four hours post instillation, BAL and biopsies were collected from challenged lung segments. Total RNA of cells from BAL and biopsy samples were sequenced and analysed for differentially expressed genes (DEGs). After challenge with LPS compared with saline, 6316 DEGs were upregulated and 241 were downregulated in BAL, but only one DEG was downregulated in biopsy samples. Upregulated DEGs in BAL were related to molecular functions such as "Inflammatory response" or "chemokine receptor activity", and upregulated pro-inflammatory pathways such as "Wnt-"/"Ras-"/"JAK-STAT" "-signaling pathway". Furthermore, the segmental LPS challenge model resembled aspects of the five most prevalent respiratory diseases chronic obstructive pulmonary disease (COPD), asthma, pneumonia, tuberculosis and lung cancer and featured similarities with acute exacerbations in COPD (AECOPD) and community-acquired pneumonia. Overall, our study provides extensive information about the transcriptomic profile from BAL cells and mucosal biopsies following LPS challenge in healthy smokers. It expands the knowledge about the LPS challenge model providing potential overlap with respiratory diseases in general and infection-triggered respiratory insults such as AECOPD in particular.

Indexed as

AsthmaPneumoniaPulmonary Disease, Chronic ObstructiveBronchoalveolar Lavage FluidEndotoxinsGene Expression ProfilingHumansLipopolysaccharidesLungEndotoxinsLipopolysaccharides

Identifiers

PMID38242945
PMCPMC10798985
OpenAlexW4391023770

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.