Background: Bronchial asthma is characterized by persistent airway inflammation and immune dysregulation. The stellate ganglion (SG), a crucial sympathetic hub, may modulate pulmonary inflammation, but the feasibility and molecular mechanisms of non-invasive modulation via infrared polarized light (IPL) remain unexplored. This study investigated the therapeutic effects and molecular basis of SG-IPL treatment in an ovalbumin (OVA)-induced asthma mouse model. Methods: BALB/c mice were divided into Control, OVA, and OVA+SG-IPL groups. The OVA+SG-IPL group received IPL irradiation on the SG region during the OVA challenge phase. Bronchoalveolar lavage fluid (BALF) cytokines IL-4, IL-5, and IL-13 were measured by ELISA. Lung histopathology was assessed using hematoxylin-eosin (H&E) and periodic acid-Schiff (PAS) staining. High-throughput RNA sequencing was performed to explore transcriptomic changes. Results: OVA-induced mice exhibited significant pulmonary inflammation, goblet cell hyperplasia, and elevated BALF cytokines (P < 0.0001). SG-IPL treatment significantly reduced these pathological changes and cytokine levels (P < 0.001). Transcriptomic analysis revealed SG-IPL broadly suppressed inflammatory pathway genes, including TNF, IL-6, IL-1β, IL-4, IL-5, and IL-13, with concurrent upregulation of anti-inflammatory regulator SIRT1. Conclusion: Non-invasive SG modulation with IPL effectively mitigated asthmatic airway inflammation, decreased Th2 cytokines, and restored lung pathology. Mechanistically, SG-IPL exerts therapeutic effects by systemically suppressing inflammatory signaling networks, notably NF-κB and TNF pathways, potentially driven by SIRT1 activation. These findings provide foundational evidence supporting neuromodulation as an innovative therapeutic approach for asthma.