Abstract

BackgroundInflammatory bowel diseases are associated with increased adiponectin (APN) levels, which may exert pro-inflammatory effects in these individuals. Since habitual exercise may increase APN, the aim of this study was to determine how exercise training affects mice with acute colitis.MethodsMale adiponectin knock out (APNKO) and wild type (WT) mice (C57BL/6) were randomly assigned to 4 different groups: 1) Sedentary (SED); 2) Exercise trained (ET); 3) Sedentary with dextran sodium sulfate (DSS) treatment (SED + DSS); and 4) Exercise trained with DSS (ET + DSS). Exercise-trained mice ran at 18 m/min for 60 min, 5d/wk for 4 weeks. Subsequently, the ET + DSS and the SED + DSS mice received 2% DSS in their drinking water for 5 days (d), followed by 5d of regular water.ResultsThe clinical symptoms of acute colitis (diarrhea, stool haemoccult, and weight loss) were unaffected by exercise and there was no difference between the APNKO and WT mice (p > 0.05) except on day 39. However, the clinical symptoms of the DSS-treated APNKO mice were worse than WT mice treated with DSS and had increased susceptibility to intestinal inflammation due to increased local STAT3 activation, higher IL-6, TNF-α, IL-1β and IL-10 levels, and as a result had increased intestinal epithelial cell proliferation (p < 0.05). Exercise training significantly decreased pro-inflammatory cytokines including IL-6, TNF-α and IL-1β (p < 0.05) in the DSS + EX APNKO mice but had no effect on epithelial cell proliferation. Exercise was also found to significantly decrease the phosphorylation expression of STAT3 in both WT and APNKO mice in DSS + EX group when compared to DSS + SED.ConclusionsExercise training may contribute in alleviating the symptoms of acute colitis and APN deficiency may exacerbate the intestinal inflammation in DSS-induced colitis.

Highlights

  • Inflammatory bowel diseases are associated with increased adiponectin (APN) levels, which may exert pro-inflammatory effects in these individuals

  • Exercise training may contribute in alleviating the symptoms of acute colitis and APN deficiency may exacerbate the intestinal inflammation in DSS-induced colitis

  • Several pro-inflammatory cytokines such as IL-1β, IL-6 and TNF-α produced by T cells, macrophages, epithelial and mesenchymal cells play a key role in the modulation of the intestinal immune system to induce, amplify and perpetuate inflammation in these individuals [4]

Read more

Summary

Introduction

Inflammatory bowel diseases are associated with increased adiponectin (APN) levels, which may exert pro-inflammatory effects in these individuals. APN is structurally homologous to collagen VIII, X, complement factor C1q [12] and the TNF family [13], and plays an important role in inflammation and the immune system [10] through the regulation of both cytokine production and their resultant systemic effects [14,15,16]. In chronic inflammatory or autoimmune diseases such as IBD and arthritis, where there is a tendency towards a negative energy balance, APN may contribute a paradoxical pro-inflammatory effect through the induction of pro-inflammatory cytokine and chemokine production such as IL-6, IL-1β, TNF-α, IL-8, granulocyte-macrophage colony stimulating factor, and monocyte chemotactic protein-1 [6,7,8]. APN binds to and inhibits certain protective growth factors such as heparin binding epidermal growth factor (HB-EGF) and basic fibroblast growth factor (bFGF), necessary for maintaining colonic epithelial cell integrity and proliferation, and regulating adhesion molecule expression and NFκB activation [6,7,8]

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call