ArticleJournal, genetic engineering & biotechnology2025
A causal relationship between circulating immune cells, plasma metabolites, and pulmonary diseases: a mediated Mendelian randomization study.
Article in Journal, genetic engineering & biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune cells and plasma metabolites may play important roles in the development of pulmonary diseases, but the relationship between different immune cells, plasma metabolites and various pulmonary diseases is still unclear. In this study, we aim to employ Mendelian randomization (MR) to investigate the causality between immune cells, pulmonary diseases and plasma metabolites.
methodsWe analyzed immune cells and seven pulmonary diseases, including interstitial lung disease (ILD), idiopathic pulmonary fibrosis (IPF), lung cancer, pneumonia, chronic obstructive pulmonary disease (COPD), sleep apnea syndrome (SAS), and tuberculosis (TB), using genome-wide association analysis (GWAS) data for immune cells as an exposure factor and seven lung diseases as outcomes. Plasma metabolites GWAS data served as mediators. We applied MR analysis to explore the relationship between immune cells and pulmonary diseases, followed by two-step mediation analysis to identify potential metabolites that may mediate this association.
resultsAs shown in the results, immune cells contribute to disease progression by reducing the protective effect of metabolites on disease or enhancing the promoting effect of metabolites on disease. These include CD4/CD8br and lung cancer, CD62L-CD86+ myeloid DC AC and Pneumonia, and Naive DN (CD4-CD8-) %T cell and COPD. On the other hand, immune cells suppress disease by increasing the inhibitory effect of metabolites on disease or decreasing the promoting effect of metabolites on disease, These include CD39 on CD39+ CD8br and ILD, CD28+ CD45RA+ CD8br AC and TB, Activated & secreting Treg AC and SAS, HLA DR on DC and IPF.
conclusionsWe clarify the importance of the potential mechanisms pertaining to immune cells, metabolites, and pulmonary diseases, highlighting the complex interactions among these factors. This understanding may assist in the diagnosis and treatment of patients with pulmonary diseases.
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.