Anne Mohr Drewes

Vagal influences in rheumatoid arthritis

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisReviewForskningpeer review

Standard

Vagal influences in rheumatoid arthritis. / Rasmussen, S. E.; Pfeiffer-Jensen, M.; Drewes, A. M. et al.
I: Scandinavian Journal of Rheumatology, Bind 47, Nr. 1, 01.2018, s. 1-11.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisReviewForskningpeer review

Harvard

Rasmussen, SE, Pfeiffer-Jensen, M, Drewes, AM, Farmer, AD, Deleuran, BW, Stengaard-Pedersen, K, Brock, B & Brock, C 2018, 'Vagal influences in rheumatoid arthritis', Scandinavian Journal of Rheumatology, bind 47, nr. 1, s. 1-11. https://doi.org/10.1080/03009742.2017.1314001

APA

Rasmussen, S. E., Pfeiffer-Jensen, M., Drewes, A. M., Farmer, A. D., Deleuran, B. W., Stengaard-Pedersen, K., Brock, B., & Brock, C. (2018). Vagal influences in rheumatoid arthritis. Scandinavian Journal of Rheumatology, 47(1), 1-11. https://doi.org/10.1080/03009742.2017.1314001

CBE

Rasmussen SE, Pfeiffer-Jensen M, Drewes AM, Farmer AD, Deleuran BW, Stengaard-Pedersen K, Brock B, Brock C. 2018. Vagal influences in rheumatoid arthritis. Scandinavian Journal of Rheumatology. 47(1):1-11. https://doi.org/10.1080/03009742.2017.1314001

MLA

Rasmussen, S. E. et al. "Vagal influences in rheumatoid arthritis". Scandinavian Journal of Rheumatology. 2018, 47(1). 1-11. https://doi.org/10.1080/03009742.2017.1314001

Vancouver

Rasmussen SE, Pfeiffer-Jensen M, Drewes AM, Farmer AD, Deleuran BW, Stengaard-Pedersen K et al. Vagal influences in rheumatoid arthritis. Scandinavian Journal of Rheumatology. 2018 jan.;47(1):1-11. doi: 10.1080/03009742.2017.1314001

Author

Rasmussen, S. E. ; Pfeiffer-Jensen, M. ; Drewes, A. M. et al. / Vagal influences in rheumatoid arthritis. I: Scandinavian Journal of Rheumatology. 2018 ; Bind 47, Nr. 1. s. 1-11.

Bibtex

@article{93659e01e540401491a33d19ea1f5682,
title = "Vagal influences in rheumatoid arthritis",
abstract = "Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease with a prevalence of 0.5–1% in Western populations. Conventionally, it is treated with therapeutic interventions that include corticosteroids, disease-modifying anti-rheumatic drugs, and biological agents. RA exerts a significant socio-economic burden and despite the use of existing treatments some patients end up with disabling symptoms. The autonomic nervous system (ANS) is a brain–body interface that serves to regulate homeostasis by integrating the external environment with the internal milieu. The main neural substrate of the parasympathetic branch of the ANS is the vagus nerve (VN). The discovery of the role of the ANS and the VN in mediating and dampening the inflammatory response has led to the proposal that modulation of neural circuits may serve as a valuable therapeutic tool. Recent studies have explored the role of the VN in this inflammatory reflex and have provided evidence that stimulation may represent a novel new therapeutic intervention. Accumulating evidence suggests that modulation of the parasympathetic tone results in a broad physiological multi-level response, including decreased pro-inflammatory cytokine response in terms of tumour necrosis factor-α, interleukin-1 (IL-1), and IL-6, and may result in an enhanced macrophage switch from M1 to M2 cells and potentially an increased level of the anti-inflammatory cytokine IL-10. Therefore, therapeutic electrical modulation of the VN may serve as an alternative, non-pharmacological, neuroimmunomodulatory intervention in RA in the future. This review gives a focused introduction to the mechanistic link between the ANS and the immune system.",
author = "Rasmussen, {S. E.} and M. Pfeiffer-Jensen and Drewes, {A. M.} and Farmer, {A. D.} and Deleuran, {B. W.} and K. Stengaard-Pedersen and B. Brock and Christina Brock",
year = "2018",
month = jan,
doi = "10.1080/03009742.2017.1314001",
language = "English",
volume = "47",
pages = "1--11",
journal = "Scandinavian Journal of Rheumatology",
issn = "0300-9742",
publisher = "Taylor & Francis ",
number = "1",

}

RIS

TY - JOUR

T1 - Vagal influences in rheumatoid arthritis

AU - Rasmussen, S. E.

AU - Pfeiffer-Jensen, M.

AU - Drewes, A. M.

AU - Farmer, A. D.

AU - Deleuran, B. W.

AU - Stengaard-Pedersen, K.

AU - Brock, B.

AU - Brock, Christina

PY - 2018/1

Y1 - 2018/1

N2 - Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease with a prevalence of 0.5–1% in Western populations. Conventionally, it is treated with therapeutic interventions that include corticosteroids, disease-modifying anti-rheumatic drugs, and biological agents. RA exerts a significant socio-economic burden and despite the use of existing treatments some patients end up with disabling symptoms. The autonomic nervous system (ANS) is a brain–body interface that serves to regulate homeostasis by integrating the external environment with the internal milieu. The main neural substrate of the parasympathetic branch of the ANS is the vagus nerve (VN). The discovery of the role of the ANS and the VN in mediating and dampening the inflammatory response has led to the proposal that modulation of neural circuits may serve as a valuable therapeutic tool. Recent studies have explored the role of the VN in this inflammatory reflex and have provided evidence that stimulation may represent a novel new therapeutic intervention. Accumulating evidence suggests that modulation of the parasympathetic tone results in a broad physiological multi-level response, including decreased pro-inflammatory cytokine response in terms of tumour necrosis factor-α, interleukin-1 (IL-1), and IL-6, and may result in an enhanced macrophage switch from M1 to M2 cells and potentially an increased level of the anti-inflammatory cytokine IL-10. Therefore, therapeutic electrical modulation of the VN may serve as an alternative, non-pharmacological, neuroimmunomodulatory intervention in RA in the future. This review gives a focused introduction to the mechanistic link between the ANS and the immune system.

AB - Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease with a prevalence of 0.5–1% in Western populations. Conventionally, it is treated with therapeutic interventions that include corticosteroids, disease-modifying anti-rheumatic drugs, and biological agents. RA exerts a significant socio-economic burden and despite the use of existing treatments some patients end up with disabling symptoms. The autonomic nervous system (ANS) is a brain–body interface that serves to regulate homeostasis by integrating the external environment with the internal milieu. The main neural substrate of the parasympathetic branch of the ANS is the vagus nerve (VN). The discovery of the role of the ANS and the VN in mediating and dampening the inflammatory response has led to the proposal that modulation of neural circuits may serve as a valuable therapeutic tool. Recent studies have explored the role of the VN in this inflammatory reflex and have provided evidence that stimulation may represent a novel new therapeutic intervention. Accumulating evidence suggests that modulation of the parasympathetic tone results in a broad physiological multi-level response, including decreased pro-inflammatory cytokine response in terms of tumour necrosis factor-α, interleukin-1 (IL-1), and IL-6, and may result in an enhanced macrophage switch from M1 to M2 cells and potentially an increased level of the anti-inflammatory cytokine IL-10. Therefore, therapeutic electrical modulation of the VN may serve as an alternative, non-pharmacological, neuroimmunomodulatory intervention in RA in the future. This review gives a focused introduction to the mechanistic link between the ANS and the immune system.

UR - http://www.scopus.com/inward/record.url?scp=85041131252&partnerID=8YFLogxK

U2 - 10.1080/03009742.2017.1314001

DO - 10.1080/03009742.2017.1314001

M3 - Review

C2 - 28766392

AN - SCOPUS:85041131252

VL - 47

SP - 1

EP - 11

JO - Scandinavian Journal of Rheumatology

JF - Scandinavian Journal of Rheumatology

SN - 0300-9742

IS - 1

ER -