Forced treadmill exercise training exacerbates inflammation and causes mortality while voluntary wheel training is protective in a mouse model of colitis

Marc D. Cook, Stephen A. Martin, Collette Williams, Keith Whitlock, Matthew A. Wallig, Brandt D. Pence, Jeffrey A. Woods

Research output: Contribution to journalArticle

Abstract

The purpose of this study was to examine whether exercise training reduced inflammation and symptomology in a mouse model of colitis. We hypothesized that moderate forced treadmill running (FTR) or voluntary wheel running (VWR) would reduce colitis symptoms and colon inflammation in response to dextran sodium sulfate (DSS). Male C57Bl/6J mice were randomized to sedentary, moderate intensity FTR (8-12. m/min, 40. min, 6. weeks, 5x/week), or VWR (30. days access to wheels). DSS was given at 2% (w/v) in drinking water over 5. days. Mice discontinued exercise 24. h prior to and during DSS treatment. Colons were harvested on Days 6, 8 and 12 in FTR and Day 8 post-DSS in VWR experiments. Contrary to our hypothesis, we found that moderate FTR exacerbated colitis symptomology and inflammation as measured by significant (p< 0.05) increases in diarrhea and IL-6, IL-1β, IL-17 colon gene expression. We also observed higher mortality (3/10 died vs. 0/10, p= 0.07) in the FTR/DSS group. In contrast, VWR alleviated colitis symptoms and reduced inflammatory gene expression in the colons of DSS-treated mice (p< 0.05). While DSS treatment reduced food/fluid intake and body weight, there was a tendency for FTR to exacerbate, and for VWR to attenuate, this effect. FTR (in the absence of DSS) increased gene expression of the chemokine and antibacterial protein CCL6 suggesting that FTR altered gut homeostasis that may be related to the exaggerated response to DSS. In conclusion, we found that FTR exacerbated, whereas VWR attenuated, symptoms and inflammation in response to DSS.

Original languageEnglish (US)
Pages (from-to)46-56
Number of pages11
JournalBrain, Behavior, and Immunity
Volume33
DOIs
StatePublished - Oct 1 2013

Fingerprint

Colitis
Running
Dextran Sulfate
Exercise
Inflammation
Mortality
Colon
Gene Expression
Interleukin-17
Interleukin-1
Chemokines
Drinking Water
Diarrhea
Interleukin-6
Homeostasis

Keywords

  • Colitis
  • Dextran sodium sulphate
  • Exercise
  • Inflammation
  • Inflammatory bowel disease
  • Serum amyloid A
  • Stress
  • Treadmill running
  • Voluntary wheel running

ASJC Scopus subject areas

  • Immunology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience

Cite this

Forced treadmill exercise training exacerbates inflammation and causes mortality while voluntary wheel training is protective in a mouse model of colitis. / Cook, Marc D.; Martin, Stephen A.; Williams, Collette; Whitlock, Keith; Wallig, Matthew A.; Pence, Brandt D.; Woods, Jeffrey A.

In: Brain, Behavior, and Immunity, Vol. 33, 01.10.2013, p. 46-56.

Research output: Contribution to journalArticle

Cook, Marc D. ; Martin, Stephen A. ; Williams, Collette ; Whitlock, Keith ; Wallig, Matthew A. ; Pence, Brandt D. ; Woods, Jeffrey A. / Forced treadmill exercise training exacerbates inflammation and causes mortality while voluntary wheel training is protective in a mouse model of colitis. In: Brain, Behavior, and Immunity. 2013 ; Vol. 33. pp. 46-56.
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abstract = "The purpose of this study was to examine whether exercise training reduced inflammation and symptomology in a mouse model of colitis. We hypothesized that moderate forced treadmill running (FTR) or voluntary wheel running (VWR) would reduce colitis symptoms and colon inflammation in response to dextran sodium sulfate (DSS). Male C57Bl/6J mice were randomized to sedentary, moderate intensity FTR (8-12. m/min, 40. min, 6. weeks, 5x/week), or VWR (30. days access to wheels). DSS was given at 2{\%} (w/v) in drinking water over 5. days. Mice discontinued exercise 24. h prior to and during DSS treatment. Colons were harvested on Days 6, 8 and 12 in FTR and Day 8 post-DSS in VWR experiments. Contrary to our hypothesis, we found that moderate FTR exacerbated colitis symptomology and inflammation as measured by significant (p< 0.05) increases in diarrhea and IL-6, IL-1β, IL-17 colon gene expression. We also observed higher mortality (3/10 died vs. 0/10, p= 0.07) in the FTR/DSS group. In contrast, VWR alleviated colitis symptoms and reduced inflammatory gene expression in the colons of DSS-treated mice (p< 0.05). While DSS treatment reduced food/fluid intake and body weight, there was a tendency for FTR to exacerbate, and for VWR to attenuate, this effect. FTR (in the absence of DSS) increased gene expression of the chemokine and antibacterial protein CCL6 suggesting that FTR altered gut homeostasis that may be related to the exaggerated response to DSS. In conclusion, we found that FTR exacerbated, whereas VWR attenuated, symptoms and inflammation in response to DSS.",
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