ArticleCellular & molecular immunology2026
Cathepsin C orchestrates RSV-induced asthma exacerbation through the dual effect of monocyte-derived macrophages.
Article in Cellular & molecular immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Combined fat and sugar intake reshapes the tumor microenvironment through hypoxia and lipogenic pathways in breast cancer.European journal of nutrition · 2026Article
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Authors and funding
16 authors.
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Abstract
Asthma exacerbations (AEs), especially those triggered by respiratory syncytial virus (RSV), remain clinically intractable because of limited treatment options and significant immune heterogeneity. In this study, we investigated the central cellular and molecular mechanisms driving RSV-induced AEs using a house dust mite-sensitized mouse model. Through macrophage depletion, transcriptomic profiling, and pathway inhibition, we identified monocyte-derived macrophages (Mo-Mφs) as key orchestrators of both antiviral responses and inflammatory amplification. Mechanistically, Mo-Mφs upregulate and secrete cathepsin C (CTSC), which in turn activates a previously unrecognized PR3/p38/RELB signaling axis. This axis established a positive feedback loop, sustaining macrophage activation and pathogenic inflammation. Pharmacological inhibition of CTSC disrupted this loop, leading to reduced lung inflammation, mucus hypersecretion, and airway hyperresponsiveness. However, this intervention was accompanied by a measurable compromise in antiviral immunity. This study reveals a previously unrecognized CTSC-driven positive feedback loop in Mo-Mφs as a core pathogenic mechanism underlying RSV-induced AE. These findings identify CTSC as a promising mechanism-based therapeutic target, highlighting the need to carefully balance inflammation control against the preservation of antiviral immunity.
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