Abstract

Recent studies demonstrated a critical functional connection between the autonomic (sympathetic and parasympathetic) nervous and the immune systems. The carotid sinus nerve (CSN) conveys electrical signals from the chemoreceptors of the carotid bifurcation to the central nervous system where the stimuli are processed to activate sympathetic and parasympathetic efferent signals. Here, we reported that chemoreflex activation via electrical CSN stimulation, in conscious rats, controls the innate immune response to lipopolysaccharide attenuating the plasma levels of inflammatory cytokines such as tumor necrosis factor (TNF), interleukin 1β (IL-1β) and interleukin 6 (IL-6). By contrast, the chemoreflex stimulation increases the plasma levels of anti-inflammatory cytokine interleukin 10 (IL-10). This chemoreflex anti-inflammatory network was abrogated by carotid chemoreceptor denervation and by pharmacological blockade of either sympathetic - propranolol - or parasympathetic - methylatropine – signals. The chemoreflex stimulation as well as the surgical and pharmacological procedures were confirmed by real-time recording of hemodynamic parameters [pulsatile arterial pressure (PAP) and heart rate (HR)]. These results reveal, in conscious animals, a novel mechanism of neuromodulation mediated by the carotid chemoreceptors and involving both the sympathetic and parasympathetic systems.

Highlights

  • Recent studies demonstrated a critical functional connection between the autonomic nervous and the immune systems

  • We investigated whether electrical carotid sinus nerve (CSN) activation in conscious rats, which activates both the baro- and chemoreflex, regulates the LPS-induced systemic inflammation

  • Our results show that CSN stimulation significantly attenuated the LPS-induced plasma levels of inflammatory cytokines including tumor necrosis factor (TNF), interleukin 1β (IL-1β), and interleukin 6 (IL-6)

Read more

Summary

Introduction

Recent studies demonstrated a critical functional connection between the autonomic (sympathetic and parasympathetic) nervous and the immune systems. The chemoreflex stimulation as well as the surgical and pharmacological procedures were confirmed by real-time recording of hemodynamic parameters [pulsatile arterial pressure (PAP) and heart rate (HR)] These results reveal, in conscious animals, a novel mechanism of neuromodulation mediated by the carotid chemoreceptors and involving both the sympathetic and parasympathetic systems. In addition to the parasympathetic vagus nerve[3, 6, 7], a recent study proposed a sympathetic regulation of the immune system[8] These authors proposed a “splanchnic anti-inflammatory pathway” modulating systemic inflammation in experimental endotoxemia. Of general anesthesia and the elimination of higher central nervous system control of the cardiovascular system[9] These collateral effects significantly attenuate the arterial baroreflex[11,12,13,14,15]. Electric CSN-stimulation combined with selective denervation of the carotid chemoreceptors[20, 24, 25] allows us to define the relative role of the sympathetic and parasympathetic system in modulating systemic inflammation

Methods
Results
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