Abstract | INTRODUCTION: Severe injury can cause intestinal permeability through decreased expression of tight junction proteins, resulting in systemic inflammation. Activation of the parasympathetic nervous system after shock through vagal nerve stimulation is known to have potent anti-inflammatory effects; however, its effects on modulating intestinal barrier function are not fully understood. We postulated that vagal nerve stimulation improves intestinal barrier integrity after severe burn through an efferent signaling pathway, and is associated with improved expression and localization of the intestinal tight junction protein occludin. METHODS: Male balb/c mice underwent right cervical vagal nerve stimulation for 10 minutes immediately before 30% total body surface area, full-thickness steam burn. In a separate arm, animals underwent abdominal vagotomy at the gastroesophageal junction before vagal nerve stimulation and burn. Intestinal barrier injury was assessed by permeability to 4 kDa FITC-dextran, histology, and changes in occludin expression using immunoblotting and confocal microscopy. RESULTS: CONCLUSION:
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Authors | Todd W Costantini, Vishal Bansal, Carrie Y Peterson, William H Loomis, James G Putnam, Fermin Rankin, Paul Wolf, Brian P Eliceiri, Andrew Baird, Raul Coimbra |
Journal | The Journal of trauma
(J Trauma)
Vol. 68
Issue 6
Pg. 1349-54; discussion 1354-6
(Jun 2010)
ISSN: 1529-8809 [Electronic] United States |
PMID | 20539179
(Publication Type: Journal Article)
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Chemical References |
- Dextrans
- Membrane Proteins
- Occludin
- Ocln protein, mouse
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Topics |
- Analysis of Variance
- Animals
- Burns
(metabolism, physiopathology)
- Dextrans
(pharmacokinetics)
- Immunoblotting
- Intestinal Mucosa
(metabolism)
- Intestines
(physiopathology)
- Male
- Membrane Proteins
(metabolism)
- Mice
- Mice, Inbred BALB C
- Microscopy, Confocal
- Occludin
- Permeability
- Signal Transduction
- Tight Junctions
(metabolism)
- Vagus Nerve Stimulation
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