Brain, behavior, and immunity
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The regulation of the innate immune response is critical for controlling inflammation and for the prevention and treatment of diseases. We recently demonstrated that the efferent vagus nerve inhibits pro-inflammatory cytokine release and protects against systemic inflammation, and termed this vagal function "the cholinergic anti-inflammatory pathway." The discovery that the innate immune response is regulated partially through this neural pathway provides a new understanding of the mechanisms that control inflammation. In this review, we outline the cholinergic anti-inflammatory pathway and summarize the current insights into the mechanisms of cholinergic modulation of inflammation. We also discuss possible clinical implications of vagus nerve stimulation and cholinergic modalities in the treatment of inflammatory diseases.
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Brain Behav. Immun. · Nov 2005
Comparative StudyThe effects of lipopolysaccharide and lithium chloride on the ingestion of a bitter-sweet taste: comparing intake and palatability.
Activation of the immune system with lipopolysaccharide (LPS) has been shown to result in decreased consumption of normally preferred substances while at the same time not affecting palatability. The present study examined the effects LPS administration on both intake and palatability of a relatively unpalatable bitter-sweet taste. Bitter is thought to signal a danger cue to an animal representing a potential toxin-containing food. ⋯ When the consummatory responses were examined, LPS-treatment produced an increase in active oral rejection relative to NaCl- and LiCl-treated groups on both conditioning days. The present study demonstrates that although both LPS- and LiCl-treatment result in similar conditioned avoidance using an intake measure, they do not elicit similar patterns of taste reactivity responding to intraoral infusions of the bitter-sweet taste. Furthermore, the present results suggest that immune activation with LPS-treatment results in increased rejection of a mildly aversive stimulus and supports the hypothesis that reorganization of behavioral priorities occurs during bacteria-induced sickness.