ArticleTheranostics2026
Attenuation of cGAS-STING signaling-mediated lung inflammation during infection through autophagy induction by bioactive nanodevices.
Article in Theranostics, 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: Modulating the cGAS-STING pathway by bioactive nanodevices is a promising strategy for combating infection-associated inflammatory disorders. However, the development of pharmacological inhibitors for cGAS-STING signaling is currently hindered by lacking cell-specific targeting capability. This study aimed to develop a potent, drug-free nanodevice that specifically targets pulmonary macrophages to modulate the cGAS-STING pathway for ameliorating infection-associated detrimental lung inflammation. Methods: Cigarette smoke extract-modified peptide gold nanoparticle hybrids (CSE-P12) were synthesized. Transcriptomic analysis, western blotting, autophagy reporter assays, and confocal microscopy were employed to assess the effects of CSE-P12 on gene expression, STING degradation, autophagic flux, and inflammation. TEM imaging and LC-MS/MS were utilized to elucidate the molecular mechanisms underlying CSE-P12-induced autophagy in macrophages. Finally, the HAdV4-induced pneumonia and CLP-induced sepsis models on wild-type and STING Results: CSE-P12 nanodevices are extensively internalized by macrophages via energy-dependent cellular uptake. This large internalization triggers autophagic degradation of STING, thereby effectively inhibiting the cGAS-STING-mediated interferon responses and inflammation. In the HAdV4-induced viral pneumonia mouse model, intratracheally instilled CSE-P12 effectively targets pulmonary macrophages, suppresses STING activation, and significantly alleviates lung inflammation and injury. The depletion of the pulmonary macrophages abolishes these protective effects. The therapeutic potential of CSE-P12 is further validated in a CLP-induced polymicrobial sepsis mouse model, where it significantly prolongs mouse survival and decreases lung inflammation. Conclusions: CSE-P12 effectively targets pulmonary macrophages and exhibits potent anti-inflammatory activities in viral pneumonia and sepsis-induced acute lung injury by inducing autophagic flux to facilitate STING degradation. This work provides a new paradigm for designing targeted nanotherapeutics to modulate STING activation in inflammatory diseases.
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