Brain–immune interactions and the neural basis of disease-avoidant ingestive behaviour

Abstract

Neuro-immune interactions are widely manifested in animal physiology. Since immunity competes for energy with other physiological functions, it is subject to a circadian trade-off between other energy-demanding processes, such as neural activity, locomotion and thermoregulation. When immunity is challenged, this trade-off is tilted to an adaptive energy protecting and reallocation strategy that is identified as 'sickness behaviour'. We review diverse disease-avoidant behaviours in the context of ingestion, indicating that several adaptive advantages have been acquired by animals (including humans) during phylogenetic evolution and by ontogenetic experiences: (i) preventing waste of energy by reducing appetite and consequently foraging/hunting (illness anorexia), (ii) avoiding unnecessary danger by promoting safe environments (preventing disease encounter by olfactory cues and illness potentiation neophobia), (iii) help fighting against pathogenic threats (hyperthermia/somnolence), and (iv) by associative learning evading specific foods or environments signalling danger (conditioned taste avoidance/aversion) and/or at the same time preparing the body to counteract by anticipatory immune responses (conditioning immunomodulation). The neurobiology behind disease-avoidant ingestive behaviours is reviewed with special emphasis on the body energy balance (intake versus expenditure) and an evolutionary psychology perspective.

The Regulation of Immunological Processes by Peripheral Neurons in Homeostasis and Disease

“…Norepinephrine has chemotactic effects on migrating extravascular monocytes and macrophages [110]. Moreover, the sympathetic tone regulates leukocyte abundance and distribution, presumably to provide anticipatory immunity during periods of peak activity when individuals are at a greater risk for pathogen exposure [111–113]. Sympathetic nerves transmitting circadian cues from the CNS entrain circadian rhythmicity on tissues by connecting the central clock of the suprachiamsatic nucleus with the peripheral clock in each tissue [114].…”

CD40-TNF activation in mice induces extended sickness behavior syndrome co-incident with but not dependent on activation of the kynurenine pathway

“…On days -5 to 0, one tube contained water and the other 0.5% (W/V) saccharin (as sodium salt hydrate, S1002, Sigma) solution, with the left-right positioning of the two tubes alternated across days. This extensive saccharin pre-exposure was carried out to prevent conditioned taste aversion (CTA) of saccharin to CD40AB-induced sickness (Pacheco-Lopez and Bermudez-Rattoni, 2011 Learning and memory of the association between neutral stimuli and an innately aversive stimulus can be studied using fear conditioning. This involves a neutral to-be-conditioned stimulus (CS e.g.…”

Klassische Konditionierung von Immunfunktionen: Mechanismen und klinische Relevanz

“…Die Klassische Konditionierung kann im weiten Sinne als das Lernen eines zeitlichen oder kausalen Zusammenhangs zwischen externen und internen Stimuli aufgefasst werden, welches den Organismus dazu befähigt, adäquate Antworten bereitzustellen, bevor biologisch relevante Ereignisse eintreten [ 32 ] . Eine Extinktion von zuvor Erlerntem bezeichnet nicht einfach das Vergessen im Sinne eines "Zerfalls" von Informationen.…”