Immune to Brain Communication in Adulthood

It was once thought that the brain was isolated from peripheral immune responses, however it is now accepted that the brain plays an integral role in the body’s response to inflammation, infection and/or stress. The effect of infection, mimicked experimentally by administration of bacterial lipopolysaccharide (LPS) has revealed that immune to brain communication is a critical component of a host organism’s response to infection and a collection of behavioural and metabolic adaptations are initiated over the course of the infection with the purpose of restricting the spread of a pathogen, optimising conditions for a successful immune response and preventing the spread of infection to other organisms [10]. These behaviours are mediated by an innate immune response and have been termed ‘sickness behaviours’ and include depression, reduced appetite, anhedonia, social withdrawal, reduced locomotor activity, hyperalgesia, reduced motivation, cognitive impairment and reduced memory encoding and recall [11, 12]. Metabolic adaptation to infection include fever, altered dietary intake and reduction in the bioavailability of nutrients that may facilitate the growth of a pathogen such as iron and zinc [10]. These behavioural and metabolic adaptions are evolutionary highly conserved and also occur in humans [13-15], further demonstrated by experiments where healthy volunteers are given a low dose of LPS and experience short term decline in cognition and increased depressive behaviours [16] and significant increased [11C]PBR28 binding, demonstrating microglial activation and neuroinflammation throughout the human brain following administration of LPS [17].

 
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