ArticleThe journal of trauma and acute care surgery2026
AR-R17779, an agonist of alpha-7 nicotinic acetylcholine receptor, attenuates trauma-induced lung epithelial glycocalyx injury by suppressing macrophage proinflammatory activity.
Article in The journal of trauma and acute care surgery, 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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1 citing paper in PubMed.
- Effects of Nicotine administration on α7nAChR, miR-124, STAT3, and inflammatory markers in Rat Lung Tissue.Molecular biology reports · 2026Article
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7 authors.
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Abstract
backgroundAcute lung injury (ALI) after trauma is associated with alveolar dysfunction that causes significant morbidity with limited treatment options. We have shown that AR-R17779, a small molecule agonist of the α7 nicotinic acetylcholine receptor highly expressed on macrophages, prevents lung edema in preclinical models of injury. The mechanism by which AR-R17779 attenuates trauma-induced ALI is unknown. We hypothesized that AR-R17779 decreases trauma-induced ALI by limiting macrophage activation and preventing lung epithelial glycocalyx breakdown.
methodsC57BL/6 mice underwent a polytrauma model consisting of lung contusion and liver crush injury with cohorts treated with an intraperitoneal dose of AR-R17779 (25 mg/kg) immediately following polytrauma. Lungs were harvested 24 hours postinjury for evaluation of ALI using histology and immunofluorescence of heparan sulfate (HS), a key component of the glycocalyx. In vitro coculture studies were performed to assess the impact of AR-R17779 on the activation of macrophages by lipopolysaccharide (LPS) and its effects on the lung epithelial glycocalyx by immunoblotting, enzyme-linked immunosorbent assay, and HS expression.
resultsAR-R17779 attenuated polytrauma-induced histological ALI and loss of HS from the lung epithelial glycocalyx. In vitro, AR-R17779 dose-dependently suppressed signal transducer and activator of transcription 3 phosphorylation and tumor necrosis factor release from LPS-treated macrophages. In coculture studies, treating LPS-stimulated macrophages with AR-R17779 decreased epithelial glycocalyx degradation compared with macrophages treated with LPS alone.
conclusionAR-R17779 attenuated trauma-induced ALI by preventing lung epithelial glycocalyx breakdown, which may result from the suppression of macrophage proinflammatory activity. Future research should test AR-R17779 as an adjunct to resuscitation aimed at limiting dysregulated macrophage activation and ALI after trauma.
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