ArticleRespiratory research2026
Integrated multiomics reveals a clinically relevant CXCL8-centric protein network in pediatric postinfectious bronchiolitis obliterans.
Article in Respiratory research, 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
9 authors.
Funding
Abstract
backgroundPediatric postinfectious bronchiolitis obliterans (PIBO) is a long-term sequela of severe lower respiratory tract infection. However, the underlying pathogenic mechanisms within the airways remain poorly understood.
methodsBronchoalveolar lavage fluid (BALF) from six children with PIBO and three control children was subjected to transcriptomic, proteomics and untargeted metabolomics analyses. Integrated analysis identified key differentially expressed candidates, among which protein candidates were subsequently validated by ELISAs.
resultsTranscriptomic analysis revealed altered pathways in the BALF of children with PIBO, including pathways related to epithelial differentiation, inflammatory responses, and metabolic processes involving amino acids, purines, lipids, and vitamins. Proteomic analysis further revealed epithelial injury, inflammatory activation, tissue remodeling, and metabolic dysregulation in PIBO patients. Protein-protein interaction (PPI) network analysis identified CXCL8 (interleukin-8, IL-8) as the central hub. Integrative transcriptomic-proteomic correlation analysis further revealed that CXCL8 transcript levels were correlated with the greatest number of differentially expressed proteins (DEPs). Subsequent ELISA validation confirmed elevated CXCL8 protein levels in children with PIBO, which were positively correlated with the predicted FEV1%. Furthermore, 54 proteins, including KRT19, OSM, ADAM8, and PADI2, were significantly correlated with CXCL8 expression. These proteins spanned epithelial, inflammatory, remodeling, and metabolic processes, indicating a clinically relevant network. Untargeted metabolomics analysis revealed alterations in purine, cofactors, and amino acid metabolism, with pyridoxine (vitamin B6) as the most significantly altered metabolite. Integrated multiomic analysis revealed widespread correlations between differentially expressed metabolites and proteins. Notably, putative pyridoxine expression was negatively correlated with the expression of CXCL8 and other key inflammatory proteins, which is consistent with the evidence of disrupted vitamin metabolism observed by transcriptomics. In vitro experiments further showed that pyridoxine treatment reduced CXCL8 secretion in small airway epithelial cells. Together, these findings suggest a potential link between vitamin B6 and inflammatory processes in PIBO.
conclusionsMultiomic integration revealed molecular signatures characterized by a CXCL8-centric protein network, a potential disruption of vitamin B6 homeostasis, and altered pathways involved in epithelial differentiation, immunity, and metabolism. These signatures converge on core pathogenic mechanisms within the airway microenvironment, including epithelial injury, inflammatory activation, tissue remodeling, and metabolic dysregulation. Collectively, these findings establish an integrative framework for understanding the pathogenesis of PIBO and highlight potential molecular targets for biomarker discovery and therapeutic intervention.
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.