Electroacupuncture promotes resolution of inflammation by modulating SPMs via vagus nerve activation in LPS-induced ALI.

Summary

This mechanistic study identifies a vagus–α7nAChR–LXA4 axis by which electroacupuncture enhances pro‑resolving lipid mediators, reduces lung permeability, and dampens cytokines in ALI. Macrophages mediate protection, α7nAChR is required, and preliminary patient data suggest symptom alleviation in sepsis-related ARDS.

Key Findings

• EA activated the cholinergic anti-inflammatory pathway via α7nAChR, reducing lung permeability and inflammatory cytokines in ALI.
• Lipoxin A4 (LXA4) was identified as a key specialized pro-resolving mediator increased by EA.
• α7nAChR-deficient mice lost EA-induced LXA4 regulation, confirming receptor necessity.
• BALF macrophages mediated protection; macrophage depletion abrogated LXA4-driven benefits.
• Preliminary clinical observations suggested symptom alleviation in sepsis-related ARDS with EA.

Clinical Implications

Electroacupuncture could emerge as an adjunct to promote resolution in sepsis-related ARDS, potentially monitored by SPMs like LXA4. Clinical adoption requires rigorously controlled trials with standardized EA protocols and sham controls.

Limitations

• Primary evidence is preclinical; human data are preliminary without randomized controls
• Standardization of EA parameters and sham-controlled designs are lacking

Future Directions

Conduct sham-controlled RCTs in sepsis-related ARDS; quantify SPM trajectories as pharmacodynamic biomarkers; dissect cell-specific α7nAChR signaling in human lung.