ArticleInternational archives of allergy and immunology2026
Fibroblast Heterogeneity Links Inflammatory Microenvironments to Tissue Remodeling in Chronic Rhinosinusitis.
Article in International archives of allergy and immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05598424 (Establishment of CST1 Predictive Model of Oral Glucocorticoid Therapy Sensitivity for Chronic Rhinosinusitis With Polyps), which is not on this map. Not yet cited in PubMed.
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Establishment of CST1 Predictive Model of Oral Glucocorticoid Therapy Sensitivity for Chronic Rhinosinusitis With Polyps
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Abstract
introductionChronic rhinosinusitis (CRS) is a heterogeneous inflammatory disorder with distinct endotypes and tissue remodeling. Fibroblasts contribute to extracellular matrix remodeling and immune regulation, but their heterogeneity in CRS remains unclear.
methodsPublic single-cell transcriptomic data from 21 CRS and healthy control samples were integrated with bulk RNA-sequencing data from primary fibroblasts derived from nasal polyps stimulated with phosphate-buffered saline, interferon (IFN)-γ, interleukin (IL)-4, or IL-17A. Fibroblast subsets, pseudotime trajectories, and inferred communication between fibroblasts and immune cells were analyzed. Cytokine-induced signatures were projected onto the fibroblast atlas. A subset of longitudinal RNA-seq data from the COMPASS cohort (NCT05598424) was used to validate predefined candidate marker genes, including IL-4-associated markers of the C8 subset and IL-17A-associated markers of the C5/C10 subsets, during glucocorticoid treatment across V1 (baseline), V2 (after 4 weeks of intranasal corticosteroid treatment), and V3 (after subsequent systemic glucocorticoid therapy). Temporal expression changes were assessed using linear mixed-effects models with V1-V2 and V2-V3 comparisons.
resultsTwelve transcriptionally distinct fibroblast subsets (C0-C11) were identified across CRS subtypes. C8 fibroblasts were enriched in eosinophilic CRSwNP and associated with type 2 inflammation-related genes, including CCL26 and POSTN, whereas C5 and C10 were associated with non-eosinophilic CRSwNP- and IL-17A-related inflammatory features. Pseudotime analysis suggested two trajectories from C4 toward C8 and C10, respectively. CellChat revealed bidirectional communication between fibroblasts and immune cell subsets. Cytokine stimulation induced distinct transcriptional responses: IFN-γ mainly induced antigen presentation and interferon response; IL-4 induced contraction- and cytoskeleton-related features; and IL-17A activated IL-17, nuclear factor κB, and tumor necrosis factor signaling pathways. Signature projection linked IL-4-related features mainly to C8 fibroblasts and IL-17A-related features mainly to C5 and C10 fibroblasts. Longitudinal analysis of glucocorticoid-treated patients identified a stable C8-associated transcriptional signature characterized by sustained downregulation of CCL26, POSTN, CISH, and CCL13 across V1-V3 time points.
conclusionsFibroblasts in CRS exhibit marked heterogeneity and may contribute to tissue remodeling and immune regulation in response to distinct inflammatory stimuli. The IL-4-associated C8 state and IL-17A-associated C5/C10 states may represent distinct fibroblast states associated with different CRS inflammatory microenvironments. The C8-associated transcriptional module shows stable and sustained suppression under glucocorticoid treatment.
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