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Balancing the autonomic nervous system to reduce inflammation in rheumatoid arthritis.

Abstract Imbalance in the autonomic nervous system (ANS) has been observed in many established chronic autoimmune diseases, including rheumatoid arthritis (RA), which is a prototypic immune-mediated inflammatory disease (IMID). We recently discovered that autonomic dysfunction precedes and predicts arthritis development in subjects at risk of developing seropositive RA. In addition, RA patients with relatively high vagus nerve tone (higher parasympathetic parameters, measured by heart rate variability) respond better to antirheumatic therapies. Together, these data suggest that the ANS may control inflammation in humans. This notion is supported by experimental studies in animal models of RA. We have found that stimulation of the so-called cholinergic anti-inflammatory pathway by efferent electrical vagus nerve stimulation (VNS) or pharmacological activation of the alpha7 subunit of nicotinic acetylcholine receptors (α7nAChR) improves clinical signs and symptoms of arthritis, reduces cytokine production and protects against progressive joint destruction. Conversely, increased arthritis activity was observed in alpha7nAChR knockout mice. These studies together with previous work in animal models of sepsis and other forms of inflammation provided the rationale for an experimental clinical trial in patients with RA. We could for the first time show that an implantable vagus nerve stimulator inhibits peripheral blood cytokine production in humans. VNS significantly inhibited TNF and IL-6 production and improved RA disease severity, even in some patients with therapy-resistant disease. This work strongly supports further studies using a bioelectronic approach to treat RA and other IMIDs.
PMID
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Authors

Mayor MeshTerms

Vagus Nerve Stimulation

Keywords

heart rate variability

inflammatory reflex

neuroimmunomodulation

nicotinic acetylcholine receptor type 7

prerheumatoid arthritis

Journal Title journal of internal medicine
Publication Year Start




PMID- 28547815
OWN - NLM
STAT- MEDLINE
DA  - 20170526
DCOM- 20170705
LR  - 20170705
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Linking)
VI  - 282
IP  - 1
DP  - 2017 Jul
TI  - Balancing the autonomic nervous system to reduce inflammation in rheumatoid
      arthritis.
PG  - 64-75
LID - 10.1111/joim.12626 [doi]
AB  - Imbalance in the autonomic nervous system (ANS) has been observed in many
      established chronic autoimmune diseases, including rheumatoid arthritis (RA),
      which is a prototypic immune-mediated inflammatory disease (IMID). We recently
      discovered that autonomic dysfunction precedes and predicts arthritis development
      in subjects at risk of developing seropositive RA. In addition, RA patients with 
      relatively high vagus nerve tone (higher parasympathetic parameters, measured by 
      heart rate variability) respond better to antirheumatic therapies. Together,
      these data suggest that the ANS may control inflammation in humans. This notion
      is supported by experimental studies in animal models of RA. We have found that
      stimulation of the so-called cholinergic anti-inflammatory pathway by efferent
      electrical vagus nerve stimulation (VNS) or pharmacological activation of the
      alpha7 subunit of nicotinic acetylcholine receptors (alpha7nAChR) improves
      clinical signs and symptoms of arthritis, reduces cytokine production and
      protects against progressive joint destruction. Conversely, increased arthritis
      activity was observed in alpha7nAChR knockout mice. These studies together with
      previous work in animal models of sepsis and other forms of inflammation provided
      the rationale for an experimental clinical trial in patients with RA. We could
      for the first time show that an implantable vagus nerve stimulator inhibits
      peripheral blood cytokine production in humans. VNS significantly inhibited TNF
      and IL-6 production and improved RA disease severity, even in some patients with 
      therapy-resistant disease. This work strongly supports further studies using a
      bioelectronic approach to treat RA and other IMIDs.
CI  - (c) 2017 The Association for the Publication of the Journal of Internal Medicine.
FAU - Koopman, F A
AU  - Koopman FA
AUID- ORCID: http://orcid.org/0000-0002-8622-1319
AD  - Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and
      Immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam,
      The Netherlands.
FAU - van Maanen, M A
AU  - van Maanen MA
AD  - Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and
      Immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam,
      The Netherlands.
FAU - Vervoordeldonk, M J
AU  - Vervoordeldonk MJ
AD  - Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and
      Immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam,
      The Netherlands.
AD  - Galvani Bioelectronics, Stevenage, UK.
FAU - Tak, P P
AU  - Tak PP
AD  - Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and
      Immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam,
      The Netherlands.
AD  - GlaxoSmithKline, Stevenage, UK.
AD  - University of Cambridge, Cambridge, UK.
AD  - Ghent University, Ghent, Belgium.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170526
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
SB  - IM
MH  - Animals
MH  - Arthritis, Rheumatoid/*physiopathology/*therapy
MH  - Autonomic Nervous System/*physiopathology
MH  - Humans
MH  - *Vagus Nerve Stimulation
OTO - NOTNLM
OT  - heart rate variability
OT  - inflammatory reflex
OT  - neuroimmunomodulation
OT  - nicotinic acetylcholine receptor type 7
OT  - prerheumatoid arthritis
EDAT- 2017/05/27 06:00
MHDA- 2017/07/06 06:00
CRDT- 2017/05/27 06:00
AID - 10.1111/joim.12626 [doi]
PST - ppublish
SO  - J Intern Med. 2017 Jul;282(1):64-75. doi: 10.1111/joim.12626. Epub 2017 May 26.