ArticleMicrobiology and immunology2026
Targeting Inflammatory Alarmin S100A9 Modulates Activation of Pro-Inflammatory Macrophage to Protect Nasal Epithelial Cells From LPS-Induced Epithelial-Mesenchymal Transition.
Article in Microbiology and immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Chronic rhinosinusitis with nasal polyps (CRSwNP) exhibits pronounced endotypic heterogeneity, with macrophages serving as key drivers of sustained mucosal inflammation. In this study, we identify S100A9 as a macrophage-derived alarmin that is markedly elevated in CRSwNP tissues. Integrative analyses of public bulk transcriptomic datasets and single-cell RNA-sequencing atlases demonstrated that S100A9 expression was predominantly enriched in macrophage clusters, where it showed strong co-expression with canonical M1-associated markers, while exhibiting limited expression in epithelial cell subsets. Spatial and correlation analyses further supported a close association between S100A9⁺ macrophages and epithelial barrier-related gene signatures. Functionally, shRNA-mediated silencing of S100A9 attenuated M1-like macrophage polarization, as evidenced by reduced expression of pro-inflammatory mediators and polarization markers, accompanied by a shift toward a less inflammatory macrophage phenotype. Conditioned media derived from S100A9-deficient macrophages significantly mitigated epithelial injury, leading to restoration of epithelial barrier integrity, as indicated by enhanced expression of tight junction proteins, including occludin and claudins. Importantly, S100A9 knockdown disrupted the pathogenic macrophage-epithelial inflammatory feedback loop, thereby dampening sustained inflammatory signaling and limiting epithelial barrier breakdown that perpetuates tissue damage in CRSwNP. Clinically, elevated S100A9 levels correlated with disease severity indices and effectively distinguished a macrophage-enriched inflammatory endotype of CRSwNP, highlighting S100A9 as both a mechanistic driver and a potential biomarker for disease stratification. Collectively, these findings position S100A9 as a mechanistic mediator and a promising therapeutic target for CRSwNP.
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.