Acupuncture inhibits neuroinflammation and gut microbial dysbiosis in a mouse model of Parkinson’s disease Original paper

What was studied?

Acupuncture-gut-microbiota-parkinsons-disease interactions were interrogated in a mechanistic mouse study using the MPTP toxin model of Parkinson’s disease (PD). Investigators asked whether acupuncture at GB34 and ST36 could ameliorate motor and anxiety-like behaviors while normalizing gut microbial dysbiosis and downstream neuroinflammation in the striatum and substantia nigra. Gut community structure, specific bacterial taxa, and predicted functional pathways were then linked statistically to dopaminergic integrity, neuroinflammatory markers, and behavior.

Who was studied?

Male C57BL/6 mice received intraperitoneal MPTP or saline and were randomized to no acupuncture, real acupuncture at GB34/ST36, or sham needling at non-acupoints. Group sizes ranged from 5–10 animals, allowing parallel behavioral, histologic and microbiome analyses within each cohort. Behavioral testing (cylinder, akinesia, rotarod, open field) was performed 11–12 days after MPTP. Fecal samples collected after treatment underwent 16S rRNA sequencing, and brain tissue was assessed by tyrosine hydroxylase immunohistochemistry and Western blot for glial, inflammatory and apoptotic markers.

Most important findings

Acupuncture substantially reversed MPTP-induced akinesia, rearing deficits, rotarod impairment and center avoidance in the open field, while sham needling had minimal effect. MPTP reduced striatal and nigral tyrosine hydroxylase and increased GFAP, Iba1, NF-κB, TNF-α and pro-apoptotic Bax with loss of anti-apoptotic Bcl-2; acupuncture largely normalized these measures in both regions, consistent with the immunoblots on page 12. MPTP produced a fall in alpha-diversity (Chao1, observed OTUs, Shannon) and a marked shift in beta-diversity on weighted UniFrac PCoA, with partial restoration by acupuncture, matching the distinct clustering shown in the ordination plots on page 7. At genus level, MPTP increased proinflammatory- or PD-associated taxa including Holdemania, Aestuariispira, Frisingicoccus, Desulfovibrio, Erysipelatoclostridium, Parabacteroides, Turicibacter, Marvinbryantia and Bifidobacterium, and decreased Butyricimonas, Alistipes, Gracilibacter, Oscillibacter, Flintibacter and Acutalibacter; acupuncture reversed 18 of 26 altered genera toward control levels. Correlation analyses linked Butyricimonas, Phocea and Gracilibacter positively, and Holdemania, Frisingicoccus and Aestuariispira negatively, with rotarod time, rearing and center crossings, forming candidate behavioral microbiome signatures relevant to PD progression.

Key implications

These data suggest that acupuncture acts as a system-level neuromodulator that reshapes gut microbial communities and their metabolic potential, dampens glial activation and apoptotic signaling, and preserves dopaminergic neurons in toxin-induced PD. Clinically, the work supports integrating acupuncture into multimodal PD care, particularly in patients with gastrointestinal symptoms or suspected dysbiosis, and motivates microbiome-informed patient stratification, mechanistic trials and microbiome–acupuncture combination strategies aligned with precision neuromodulation.

Citation

Jang JH, Yeom MJ, Ahn S, et al. Acupuncture inhibits neuroinflammation and gut microbial dysbiosis in a mouse model of Parkinson’s disease. Brain Behav Immun. 2020;89:641-655. doi:10.1016/j.bbi.2020.08.015