ArticleJournal of inflammation research2026
Iron Dyshomeostasis and Divergent Antigen Presentation Remodeling in Bronchiectasis: A Dual-Dataset Transcriptomic Analysis.
Article in Journal of inflammation 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.
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Abstract
Background: Bronchiectasis features persistent neutrophilic inflammation with recurrent infections, yet why abundant immune infiltrates fail to clear bacteria remains unclear. Ferroptosis-iron-dependent regulated cell death-modulates immunity in oncology but is unexplored in chronic airway diseases. Methods: We performed dual-dataset transcriptomic analysis integrating bulk lung RNA-sequencing (GSE153131: bronchiectasis, normal, pneumonia) and an in vitro BEAS-2B epithelial microarray dataset (1,004 differentially expressed genes at FDR < 0.05). Ferroptosis gene-set scoring, immune deconvolution, orthogonal neutrophil validation, and Gene Set Enrichment Analysis were conducted. Bulk tissue analysis (Dataset 1) was based on a single bronchiectasis sample and interpreted descriptively. Results: Bulk tissue showed iron dyshomeostasis (HMOX1↑, FTL↓, TFRC↑) with myeloid chemokine hyperactivation (CXCL9↑ 5.9-fold, CXCL10↑ 2.4-fold) and T-cell effector attenuation (CD3D↓ 46%, GZMB↓ 54%). PTGS2 was unchanged. In the epithelial model, ferroptosis suppressor genes were coordinately downregulated (25/39), and MHC class II machinery was significantly suppressed (CIITA↓: logFC=-0.90, P=0.022; HLA-DMA↓: logFC=-1.11, P=0.010; HLA-DMB↓: logFC=-1.12, P=0.036), while MHC class I (B2M↑) was preserved. T-cell markers were absent from epithelium, confirming interstitial origin of T-cell attenuation. Conclusion: Bronchiectasis exhibits compartment-specific iron-immune dysregulation: epithelial iron dyshomeostasis with selective MHC-II downregulation coexisting with myeloid chemokine hyperactivation. This "recruitment-presentation uncoupling" may explain the inflammation-clearance paradox. Iron-dependent dioxygenases (TET/PHD/JMJD) are proposed as intermediaries linking iron to CIITA regulation.
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