Against the Storm with the Vagus Nerve

Cytokine storm is a situation in which the response of the immune system gets out of hand, such that it actually causes more harm than good. The condition has received increased attention in the SARS-CoV2 pandemic, as it’s a serious complication of COVID-19. Cytokine storm means that there is an excessive release of cytokines flooding the body, driving the inflammation further and further. Besides in COVID, it can also occur in many other infections and diseases. But no matter what the cause, cytokine storm is always a life-threating situation.

The common antihistaminic substance famotidine was found to be helpful in some COVID patients in this situation. But how exactly the drug (which is usually used to treat stomach problems) exerts its function in COVID was unclear, so it hasn’t been widely used in this case yet. The group of Kevin Tracey at the Feinstein Institute of Bioelectronic Medicine has now found an unexpected explanation for how the drug attenuates cytokine storm: Through a neural reflex.

Two hints brought the group to their rather unconventional hypothesis: First, rather high doses of famotidine are needed to be efficient in COVID. Second, famotidine does not easily pass the blood brain barrier. In a mouse model, the authors indeed found that injections of the drug into the brain were much more efficient than into the body. Equipped with CorTec’s cuff electrodes, the group found that it was the Vagus nerve, originating in the brain stem, in which famotidine increased the neural activity. The nerve was already known to exert an anti-inflammatory reflex that helps to keep inflammations at bay. To test whether the reflex also constitutes the sought-for mechanism of action of famotidine, the authors experimentally severed the Vagus nerve before administering the drug. Indeed, without the nerve, famotidine could no longer ameliorate the inflammation.

With their research, the group seems to have uncovered a previously unknown Vagus nerve dependent anti-inflammatory pathway that mediates famotidine’s action in cytokine storm. This is an interesting demonstration of how bioelectronic probes can be instrumental in basic biomedical research above and beyond neuromodulation.

 

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Citation:

Yang H, George SJ, Thompson DA, Silverman HA, Tsaava T, Tynan A, Pavlov VA, Chang EH, Andersson U, Brines M, Chavan SS, Tracey KJ. Famotidine activates the vagus nerve inflammatory reflex to attenuate cytokine storm. Mol Med. 2022 May 16;28(1):57. doi: 10.1186/s10020-022-00483-8. PMID: 35578169; PMCID: PMC9109205.

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SPECIFICATIONS

FEATURE 

Recording channels 

Sampling rate 

Sampling dynamic range 

High pass filter cut-off 

Low pass filter cut-off 

Amplifier band pass gain 

Band pass roll-off 

Reference


Stimulation 

Stimulation channels 

Current 

Current source 

Pulse width 

Power supply 

Wireless data transmission 

Closed Loop latency

VALUE

32 

1 kHz 

16 bit (74 nV smallest increment) 

ca. 2 Hz 

325 Hz 

Adjustable: 100-750 

20 dB/dec 

Any (subset) of the recording channels selectable by software or one dedicated hard-wired additional contact 

Current-controlled, biphasic, rectangular, asymmetric stimulus pulses (cathodic amplitude with pulse width followed by an anodic counter pulse of 1/4x amplitude and 4x pulse width) 

 32 

Max. -6 mA / +1.5 mA (24 µA increments) within

 compliance voltage range of -11 V to +5 V 

Can be directed to any of the 32 electrode contacts 

Negative phase: 10 µs – 2,500 µs

Wireless inductive, 120-140 kHz

Bi-directional, radio frequency in 2400-2483.5 MHz band ≤ 40 ms