ArticleBMC pulmonary medicine2025
Transcriptomics reveals the underlying mechanism of Prostaglandin E1 in improving severe pneumonia.
Article in BMC pulmonary medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Association between blood urea nitrogen-to-creatinine ratio trajectories and mortality in patients with severe pneumonia requiring invasive mechanical ventilation: a Medical Information Mart for Intensive Care IV (MIMIC-IV) database analysis.Journal of thoracic disease · 2026Article
- Immune monitoring, immune phenotyping, and precision intervention in severe pneumonia: current evidence and translational challenges.Frontiers in immunology · 2026Review
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.
Funding
Abstract
backgroundSevere pneumonia is a lung parenchymal inflammation that can lead to multi-organ failure and death. Prostaglandin E1 (PGE1) is an autoreactive substance with extensive physiologic and pharmacologic properties. This study aims to investigate the ameliorative effect and potential mechanism of PGE1 in mice with severe pneumonia.
methodsMouse models of severe pneumonia were established by lipopolysaccharide (LPS), and the mice were administrated PGE1 to observe the effects of PGE1 on the pathological injury of lung tissues, wet-to-dry weight (W/D) ratio of lung tissues, levels of inflammatory factors in broncho-alveolar lavage fluid (BALF) and lung tissues, the number of white blood counts (WBCs) and polymorphonuclear neutrophils (PMNs) in BALF, blood gas indexes, and Th17/Treg balance. The critical signaling pathways of PGE1 involved in severe pneumonia were obtained by transcriptome sequencing (RNA-seq), and the regulatory role of PGE1 in alleviating severe pneumonia was observed by the JAK inhibitor AG490.
resultsPGE1 can alleviate lung histopathological injury in mice with severe pneumonia, decrease W/D ratio, attenuate interleukin- 1β (IL-1β), interleukin- 6 (IL-6), and tumor necrosis factor-α (TNF-α) levels, increase interleukin- 10 (IL-10) levels in mouse BALF and lung tissues, and reduce the number of WBCs and PMNs; it can increase the arterial blood partial pressure of oxygen (PaO2) and decrease the arterial blood partial pressure of carbon dioxide (PaCO2), and up-regulate the proportion of Treg cells, decrease RORγt expression, and increase Foxp3 expression. Differential gene expression analysis and enrichment analyses showed that the enrichment of JAK-STAT pathway was decreased in the LPS + PGE1 group compared to the LPS group. Joint use of PGE1 and AG490 can reduce p-JAK2 and p-STAT3 protein expression and synergistically improve the pathological damage phenotype in mice with severe pneumonia.
conclusionPGE1 can alleviate lung histopathological injury and reduce the degree of pulmonary edema in mice with severe pneumonia, and the mechanism might be realized by preventing PMN aggregation and activation in the lungs, reducing the release of inflammatory mediators, improving pulmonary ventilation, and regulating immune homeostasis. Moreover, by using transcriptome analysis and animal experiments, this study found that PGE1 participates in severe pneumonia by regulating JAK-STAT pathway.
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.