BL13 EA in asthma

Inspired by Liu et al 2025.[1]

EA – electroacupuncture
IF – impact factor
API – allergic pulmonary inflammation
SP – spinous process
CHRM3 – cholinergic receptor muscarinic 3
CHRM4 – cholinergic receptor muscarinic 4

– key to acronyms

This paper is from the British Journal of Pharmacology (IF 6.8) – a journal first established in 1946 and focussing on experimental pharmacology. I think it is the first time I have highlighted a paper from here, since acupuncture research does not usually find itself categorised under experimental pharmacology.

The research comes from Shanghai, hence the image above, and would be easily overlooked from just skimming the title. A more careful reading reveals a rare finding – that of an exacerbation of a medical condition (or a model of such) from what appears to be a reasonable (procedurally safe) treatment approach.

I remember hearing the suggestion, when I was first using medical acupuncture in the 90’s, that acupuncture might sometimes exacerbate asthma. I had nothing physiological to pin this idea to, so it was always left aside in my mind, so to speak. Since then, we have seen mortality outcomes related to EA in certain contexts. Mostly, these have been reduced mortality in models of sepsis, but we have seen an example of increased lethality with strong EA to abdominal points after the onset of sepsis. Prior to the onset of sepsis, the same stimulation was protective.[2]

This paper shares some similarities with the one I highlighted previously (see: ST36 vs ST25 EA in sepsis) and also an author. The first author on the paper in Neuron from 2020 is the last author on the current paper.

A rodent model of allergic pulmonary inflammation (API) was created by intranasal instillation of papain on 5 consecutive days. Papain is a cysteine protease enzyme derived from the papaya plant (Carica papaya). It breaks down epithelial proteins in the lungs and increases tissue permeability.

EA was applied using pairs of needles at ST36, LU5, or BL13, ie muscle in the leg, muscle in the arm (forelimb), or the Back-Shu point of the Lung. The latter is situated on the inner Bladder line at the lower border of the SP of T3, ie roughly in-between the middle of the scapulae.

EA was applied at 10Hz (50μs pulse width) for 30 minutes on consecutive days for 5 days, and at intensities of either 0, 0.1, 0.2, or 0.5mA. This was over the same period that the papain was instilled.

EA to the limbs made no difference, but EA applied at BL13 exacerbated the API and reduced survival in a dose dependant manner. The subsequent research was devoted to examining the mechanism of this effect and included looking to see which proteins were upregulated or downregulated by EA at BL13, as well as blocking local nerves and autonomic ganglia.

Ultimately, the worsening of API following EA at BL13 was attributed to an autonomic reflex involving muscarinic acetylcholine receptors (CHRM3 and CHRM4), and it could be blocked by ipratropium.

So, this research demonstrates somatovisceral (autonomic) reflexes that can exacerbate inflammation. Previously these were segmental sympathetic reflexes involving release of catecholamines; however, here we see cholinergic reflexes, principally involving the M3 and M4 acetylcholine receptors.

In terms of our human patients, it might be wise to avoid using paraspinal segmental approaches in patients with API or the equivalent (exacerbations of asthma), and favour limb muscles instead.

References

1          Liu S, Ge J, Liu W, et al. Involvement of the somatosensory-autonomic reflex and muscarinic receptors in exacerbation of allergic pulmonary inflammation by electroacupuncture. Br J Pharmacol. Published Online First: 9 February 2025. doi: 10.1111/bph.17415

2          Liu S, Wang Z-F, Su Y-S, et al. Somatotopic Organization and Intensity Dependence in Driving Distinct NPY-Expressing Sympathetic Pathways by Electroacupuncture. Neuron. 2020;108:436-450.e7. doi: 10.1016/j.neuron.2020.07.015

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Declaration of interests MC