Autonomic nervous system function predicts the inflammatory response over three years in newly diagnosed ulcerative colitis patients

V. Gunterberg, M. Simrén, L. Öhman, P. Friberg, M. P. Jones, L. Van Oudenhove, H. Strid

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Background: The autonomic nervous system (ANS) modulates intestinal inflammation in animal models. Human evidence confirming such modulating influence is limited. We aimed to investigate whether ANS function is associated with inflammatory parameters at disease onset, and whether it predicts the evolution of inflammation in patients with ulcerative colitis (UC). Methods: We prospectively monitored 51 patients from onset of UC for 3 years. Upon remission of the onset flare, ANS activity was assessed by heart rate variability analysis and compared with healthy controls. Inflammatory parameters in blood, stool, and colonic biopsies obtained at onset and during follow-up visits were analyzed. Generalized linear models were used to test cross-sectional associations between ANS activity and inflammatory parameters at onset; linear mixed models were used to test whether ANS function at onset predicted the evolution of inflammation over the following 3 years. Key Results: Sympathovagal balance was different in UC patients compared to healthy controls, and cross-sectional associated with higher levels of systemic (erythrocyte sedimentation rate [ESR], CRP, TNF-α, IFN-γ) and mucosal inflammation (interleukin-8, IFN-γ) at onset. Conversely, a negative cross-sectional association with parasympathetic activity was found for ESR & TNF-α. Longitudinally, parasympathetic activity at onset predicted systemic (ESR, WBC), but not mucosal inflammation during follow-up. Conclusions & Inferences: This study further strengthens the association between the ANS system and intestinal inflammation previously found in animal models and recently in patients with inflammatory bowel disease. These results may have important implications for the pathogenesis and treatment of UC.

LanguageEnglish
Pages1655-1662
Number of pages8
JournalNeurogastroenterology and Motility
Volume28
Issue number11
DOIs
Publication statusPublished - 1 Nov 2016

Fingerprint

Autonomic Nervous System
Ulcerative Colitis
Inflammation
Blood Sedimentation
Linear Models
Animal Models
Tumor Necrosis Factor-alpha
Interleukin-8
Inflammatory Bowel Diseases
Heart Rate
Biopsy

Keywords

  • autonomic nervous system function
  • clinical course
  • inflammation
  • ulcerative colitis

Cite this

Gunterberg, V. ; Simrén, M. ; Öhman, L. ; Friberg, P. ; Jones, M. P. ; Van Oudenhove, L. ; Strid, H. / Autonomic nervous system function predicts the inflammatory response over three years in newly diagnosed ulcerative colitis patients. In: Neurogastroenterology and Motility. 2016 ; Vol. 28, No. 11. pp. 1655-1662.
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abstract = "Background: The autonomic nervous system (ANS) modulates intestinal inflammation in animal models. Human evidence confirming such modulating influence is limited. We aimed to investigate whether ANS function is associated with inflammatory parameters at disease onset, and whether it predicts the evolution of inflammation in patients with ulcerative colitis (UC). Methods: We prospectively monitored 51 patients from onset of UC for 3 years. Upon remission of the onset flare, ANS activity was assessed by heart rate variability analysis and compared with healthy controls. Inflammatory parameters in blood, stool, and colonic biopsies obtained at onset and during follow-up visits were analyzed. Generalized linear models were used to test cross-sectional associations between ANS activity and inflammatory parameters at onset; linear mixed models were used to test whether ANS function at onset predicted the evolution of inflammation over the following 3 years. Key Results: Sympathovagal balance was different in UC patients compared to healthy controls, and cross-sectional associated with higher levels of systemic (erythrocyte sedimentation rate [ESR], CRP, TNF-α, IFN-γ) and mucosal inflammation (interleukin-8, IFN-γ) at onset. Conversely, a negative cross-sectional association with parasympathetic activity was found for ESR & TNF-α. Longitudinally, parasympathetic activity at onset predicted systemic (ESR, WBC), but not mucosal inflammation during follow-up. Conclusions & Inferences: This study further strengthens the association between the ANS system and intestinal inflammation previously found in animal models and recently in patients with inflammatory bowel disease. These results may have important implications for the pathogenesis and treatment of UC.",
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Autonomic nervous system function predicts the inflammatory response over three years in newly diagnosed ulcerative colitis patients. / Gunterberg, V.; Simrén, M.; Öhman, L.; Friberg, P.; Jones, M. P.; Van Oudenhove, L.; Strid, H.

In: Neurogastroenterology and Motility, Vol. 28, No. 11, 01.11.2016, p. 1655-1662.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Gunterberg, V.

AU - Simrén, M.

AU - Öhman, L.

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AU - Jones, M. P.

AU - Van Oudenhove, L.

AU - Strid, H.

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N2 - Background: The autonomic nervous system (ANS) modulates intestinal inflammation in animal models. Human evidence confirming such modulating influence is limited. We aimed to investigate whether ANS function is associated with inflammatory parameters at disease onset, and whether it predicts the evolution of inflammation in patients with ulcerative colitis (UC). Methods: We prospectively monitored 51 patients from onset of UC for 3 years. Upon remission of the onset flare, ANS activity was assessed by heart rate variability analysis and compared with healthy controls. Inflammatory parameters in blood, stool, and colonic biopsies obtained at onset and during follow-up visits were analyzed. Generalized linear models were used to test cross-sectional associations between ANS activity and inflammatory parameters at onset; linear mixed models were used to test whether ANS function at onset predicted the evolution of inflammation over the following 3 years. Key Results: Sympathovagal balance was different in UC patients compared to healthy controls, and cross-sectional associated with higher levels of systemic (erythrocyte sedimentation rate [ESR], CRP, TNF-α, IFN-γ) and mucosal inflammation (interleukin-8, IFN-γ) at onset. Conversely, a negative cross-sectional association with parasympathetic activity was found for ESR & TNF-α. Longitudinally, parasympathetic activity at onset predicted systemic (ESR, WBC), but not mucosal inflammation during follow-up. Conclusions & Inferences: This study further strengthens the association between the ANS system and intestinal inflammation previously found in animal models and recently in patients with inflammatory bowel disease. These results may have important implications for the pathogenesis and treatment of UC.

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