Frontiers in immunology · 2026
650 nm red-light therapy attenuates sepsis-induced acute lung injury via adiponectin-mediated immune-metabolic reprogramming.
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Zhang Yiqiu, Ni Wei, Li Jianghan, Bai Yubing, Bai Yier, Jiang Zhixuan, Wang Jiadie, He Yu, Li Yafeng, Yuan Jing, Yao Min
Аннотация
BACKGROUND: Sepsis-induced acute lung injury (ALI) is driven by dysregulated innate immunity and mitochondrial dysfunction. Monocyte/macrophage trafficking and polarization critically shape disease trajectory, yet clinically tractable immunometabolic interventions are limited. We hypothesized that 650 nm red-light photobiomodulation (PBM) alleviates septic ALI by reprogramming myeloid responses and preserving mitochondrial function via adiponectin signaling.
METHODS: Septic ALI was induced by cecal ligation and puncture (CLP) in mice. Animals received 650 nm PBM (10 min, every 6 h, three times within 24 h). Survival, lung edema, histology, and serum cytokines were assessed. Lung chemokines/cytokines were profiled by 23-plex Luminex. Immune composition was analyzed by flow cytometry, and CCR2+/CX3CR1+ subsets were visualized in CcrRFP-Cx3cr1GFP mice using 3D cryo-fMOST. IHC quantified CX3CR1, CCR2, CD68, CD86, and CD206. Adiponectin was measured in serum/BALF and lung. Pathway relevance was tested by AdipoR1 siRNA. In LPS-stimulated RAW264.7 macrophages, PBM effects on cytokines, ATP, mitochondrial ROS (MitoSOX), membrane potential (JC-1), and MitoTracker fluorescence were evaluated, with/without AdipoR1 knockdown.
RESULTS: PBM prolonged survival, reduced lung edema, improved histopathology, and lowered systemic TNF-α, IL-6, IL-1β, and MCP-1. Luminex showed broad suppression of pro-inflammatory mediators (e.g., G-/GM-CSF, IL-1 family, IL-6, IL-12, IL-17A, TNF-α) and chemokines (CCL11, CXCL1, MCP-1/CCL2, CCL3/4/5), with increases in IL-4/IL-10/IL-13. Flow cytometry revealed decreased neutrophils, monocytes, and inflammatory macrophages, alongside restored eosinophils and resident macrophages. Cryo-fMOST and IHC demonstrated reduced CCR2+/CD86+ inflammatory cells and enrichment of CX3CR1+/CD206+ reparative cells. PBM elevated adiponectin in serum, BALF, and lung; AdipoR1 knockdown abrogated anti-inflammatory effects and myeloid rebalancing. In vitro, PBM dose-dependently suppressed LPS-induced TNF-α/IL-6 and IL-1β while increasing IL-10, restored ATP, reduced mitochondrial ROS, and improved membrane potential, that benefits lost with AdipoR1 silencing.
CONCLUSIONS: Septic ALI modulated by 650 nm PBM was characterized by suppressing CCR2+ inflammatory recruitment, enriching CX3CR1+/M2-like macrophages, and preserving mitochondrial function through adiponectin-AdipoR1 signaling. These data position red-light PBM as a mechanistically grounded, non-invasive method for sepsis-associated lung injury.
METHODS: Septic ALI was induced by cecal ligation and puncture (CLP) in mice. Animals received 650 nm PBM (10 min, every 6 h, three times within 24 h). Survival, lung edema, histology, and serum cytokines were assessed. Lung chemokines/cytokines were profiled by 23-plex Luminex. Immune composition was analyzed by flow cytometry, and CCR2+/CX3CR1+ subsets were visualized in CcrRFP-Cx3cr1GFP mice using 3D cryo-fMOST. IHC quantified CX3CR1, CCR2, CD68, CD86, and CD206. Adiponectin was measured in serum/BALF and lung. Pathway relevance was tested by AdipoR1 siRNA. In LPS-stimulated RAW264.7 macrophages, PBM effects on cytokines, ATP, mitochondrial ROS (MitoSOX), membrane potential (JC-1), and MitoTracker fluorescence were evaluated, with/without AdipoR1 knockdown.
RESULTS: PBM prolonged survival, reduced lung edema, improved histopathology, and lowered systemic TNF-α, IL-6, IL-1β, and MCP-1. Luminex showed broad suppression of pro-inflammatory mediators (e.g., G-/GM-CSF, IL-1 family, IL-6, IL-12, IL-17A, TNF-α) and chemokines (CCL11, CXCL1, MCP-1/CCL2, CCL3/4/5), with increases in IL-4/IL-10/IL-13. Flow cytometry revealed decreased neutrophils, monocytes, and inflammatory macrophages, alongside restored eosinophils and resident macrophages. Cryo-fMOST and IHC demonstrated reduced CCR2+/CD86+ inflammatory cells and enrichment of CX3CR1+/CD206+ reparative cells. PBM elevated adiponectin in serum, BALF, and lung; AdipoR1 knockdown abrogated anti-inflammatory effects and myeloid rebalancing. In vitro, PBM dose-dependently suppressed LPS-induced TNF-α/IL-6 and IL-1β while increasing IL-10, restored ATP, reduced mitochondrial ROS, and improved membrane potential, that benefits lost with AdipoR1 silencing.
CONCLUSIONS: Septic ALI modulated by 650 nm PBM was characterized by suppressing CCR2+ inflammatory recruitment, enriching CX3CR1+/M2-like macrophages, and preserving mitochondrial function through adiponectin-AdipoR1 signaling. These data position red-light PBM as a mechanistically grounded, non-invasive method for sepsis-associated lung injury.