Key result
Electrical stimulation of the carotid sinus nerve in conscious rats significantly attenuated LPS-induced systemic inflammation by decreasing TNF, IL-1β, and IL-6, and increasing IL-10 via chemoreceptor activation.
Why the study?
Does carotid sinus nerve electrical stimulation attenuate systemic inflammation in conscious rats?
Does carotid sinus nerve electrical stimulation attenuate systemic inflammation in conscious rats?
Electrical stimulation of the carotid sinus nerve attenuates systemic inflammation via a novel neuromodulatory mechanism involving both sympathetic and parasympathetic systems.
Answers are grounded in this paper and cite their sources.
CSN stimulation modulates innate immunity in rats; leaves open whether this autonomic-immune link extends to human disease.
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.
No takes yet. Share an insight, caveat, or question.
Santos‐Almeida et al. (2017) studied LPS-induced systemic inflammation. Carotid sinus nerve (CSN) electrical stimulation vs. Sham/Control (no stimulation) was evaluated on Plasma levels of inflammatory cytokines (TNF, IL-1β, IL-6) and anti-inflammatory cytokine (IL-10) (p=<0.05). Electrical stimulation of the carotid sinus nerve in conscious rats significantly attenuated LPS-induced systemic inflammation by decreasing TNF, IL-1β, and IL-6, and increasing IL-10 via chemoreceptor activation.
Synapse has enriched 10 related papers. Consider them for comparative context: