ArticleBMC genomics2026
Integration of bulk RNA-seq and scRNA-seq reveals cell subsets and gene signatures associated with Glaesserella parasuis infection.
Article in BMC genomics, 2026. 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
13 authors.
Funding
Abstract
backgroundGlaesserella parasuis (GPS) is a major bacterial pathogen threatening the pig industry worldwide. It is widely prevalent in pig farms across China; however, to date, no effective strategies for its prevention and control are available. It causes divergent outcomes ranging from asymptomatic carriage to lethal disease; however, the underlying mechanisms remain unclear. In this study, we integrated bulk- and single-cell RNA-seq of over 98,000 porcine alveolar macrophages from a well-defined piglet infection model (including control, mild, and severe groups).
resultsThis is the first multi-omics dissection of macrophage heterogeneity in GPS infection at single-cell resolution. We identified four transcriptionally distinct macrophage subpopulations, with two inflammation-associated subsets (Im-Mac and Inf- Mac) that expanded dramatically with increasing disease severity. Pseudotime analysis revealed that severe infection skews macrophage differentiation almost exclusively toward pro-inflammatory fates. Integrated analysis revealed two opposing cellular programs dictating clinical outcomes: a protective program (active in mild infections, marked by CXCL10, CD69, SERPING1, and KMO) balancing immune recruitment with regulation, and a pathogenic program (dominating severe infections, characterized by a 16-gene signature including AMCF-II, CCL2, SERPINB2, CD14, ECE1, and IL7R). Notably, 9 of these 16 genes overlapped with a core set of 58 genes that were positively correlated with disease progression.
conclusionsWe propose a balanced model in which the equilibrium between protective and pathogenic macrophage programs dictates the outcome of GPS infection. These findings provide novel cell-state-specific biomarkers and a molecular framework for understanding the divergent clinical outcomes of GPS infection.
Indexed as
Identifiers
What Socratic 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 Socratic graph.