Acupuncture Mediates the Treatment of Childhood Pneumonia via Modulation of Lung ADRB2
Lingjuan Liu, Weicheng Qin, Xiaofan Xu, Anqi Zhong, Weitong Cai, Junjie Liang, Ting Yu, Haodong Su, Xiulan DongAbstract
Background
Childhood pneumonia (CP) remains a major cause of pediatric hospitalization and mortality. Antibiotic resistance and drug-related adverse reactions highlight the need for safe adjunctive treatments. The β₂-adrenergic receptor (ADRB2) is associated with airway reactivity and inflammatory responses. Acupuncture has been reported to modulate autonomic and immune functions; however, its precise molecular mechanism in CP remains unclear.
Methods
Clinical outcomes were evaluated alongside transcriptomic analyses and animal experiments. The transcriptomic analyses comprised a pediatric PBMC dataset (GSE261482) and an independent mouse lung RNA-sequencing dataset (GSE325662). An LPS-induced juvenile mouse model was established to assess lung pathology, inflammatory cytokines (TNF-α, IL-1β, IL-10), and ADRB2 expression. Salbutamol and ICI-118551 were used to examine ADRB2-related effects.
Results
Acupuncture showed significant adjunctive benefit, improving day-5 efficacy (P = 0.001), day-7 efficacy (P < 0.001), and day-5 clinical scores (P = 0.002), while shortening hospital stay (P < 0.001) without serious adverse reactions. Transcriptomic analysis implicated adrenergic signaling, particularly ADRB2, in CP. In juvenile mice, acupuncture reduced lung inflammation and modulated cytokine levels and ADRB2 expression. These findings suggest an association between ADRB2-related signalling and the pulmonary inflammatory response to acupuncture.
Conclusion
Acupuncture was associated with improved clinical outcomes in CP and attenuated lung inflammation in an LPS-induced juvenile mouse model. ADRB2-related adrenergic signaling may be involved in this anti-inflammatory effect. These results support the potential role of acupuncture as an adjunctive intervention for CP, although further studies are needed to confirm the causal contribution of ADRB2 and to define the underlying cell-specific mechanisms.