Vagotomy significantly increased mortality and elevated serum corticosterone levels in a murine model of polymicrobial sepsis, demonstrating that the vagus nerve attenuates immune dysregulation.
The particular importance of the vagus nerve for the pathophysiology of peritonitis becomes more and more apparent. In this work we provide evidence for the vagal modulation of inflammation in the murine model of colon ascendens stent peritonitis (CASP). Vagotomy significantly increases mortality in polymicrobial sepsis. This effect is not accounted for by the dilatation of gastric volume following vagotomy. As the stimulation of cholinergic receptors by nicotine has no therapeutic effect, the lack of nicotine is also not the reason for the reduced survival rate. In fact, increased septic mortality is a consequence of the absent modulating influence of the vagus nerve on the immune system: we detected significantly elevated serum corticosterone levels in vagotomised mice 24 h following CASP and a decreased ex vivo TNF-alpha secretion of Kupffer cells upon stimulation with LPS. In conclusion, the vagus nerve has a modulating influence in polymicrobial sepsis by attenuating the immune dysregulation.
Keßler et al. (2012) studied Polymicrobial sepsis. Vagotomy vs. Non-vagotomised mice was evaluated on Mortality and inflammatory markers (serum corticosterone, TNF-alpha secretion). Vagotomy significantly increased mortality and elevated serum corticosterone levels in a murine model of polymicrobial sepsis, demonstrating that the vagus nerve attenuates immune dysregulation.
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