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The cGAS–STING pathway in pulmonary infectious and sterile inflammation: differences; connections; and therapeutic implications
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DOI：10.3389/fimmu.2026.1867680.png)
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Abstract
En 中文
The cyclic GMP–AMP synthase–stimulator of interferon genes (cGAS–STING) signaling pathway plays a pivotal role in mediating both infectious and sterile pulmonary inflammation; exhibiting distinct dynamic characteristics under different contexts. The activation kinetics of the cGAS–STING pathway are highly dependent on disease context. In many acute infections; the cGAS–STING pathway is often activated rapidly and induces a strong type I interferon (IFN-I) response; which helps control pathogens. In contrast; chronic sterile injury is usually associated with endogenous damage-associated molecular patterns (DAMPs); persistent low-level pathway activation; inflammatory remodeling; and fibrosis. However; these patterns should be viewed as two ends of a dynamic infectious–sterile continuum rather than as mutually exclusive categories. In many pulmonary diseases; including tuberculosis; chronic viral infection; chronic obstructive pulmonary disease (COPD) exacerbation; infection-associated acute respiratory distress syndrome (ARDS); and post-infectious fibrosis; infectious and sterile mechanisms may coexist; overlap; or occur sequentially. This review summarizes the similarities; differences; and mechanistic connections between cGAS–STING signaling in infectious and sterile lung inflammation. We focus on upstream triggers; signaling dynamics; cell-specific responses; intercellular cyclic GMP-AMP (cGAMP) transmission; inflammatory outcomes; biomarkers; and therapeutic implications. We also propose a temporal–intensity model of cGAS–STING signaling as a conceptual framework to better understand stage-specific pathway functions and support future translational research.
Keywords:
biomarkers
infectious diseases
fibrosis
pulmonary inflammation
sterile inflammation
cGAS–STING pathway
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5.9
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4.9W
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22.7W
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