Limits...
Why Do We Feel Sick When Infected--Can Altruism Play a Role?

Shakhar K, Shakhar G - PLoS Biol. (2015)

Bottom Line: Nonetheless, SB seems evolutionarily costly: it promotes starvation and predation and reduces reproductive opportunities.Former explanations focused on individual fitness, invoking improved resistance to pathogens.Could prevention of disease transmission, propagating in populations through kin selection, also contribute to SB?

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, College of Management Academic Studies, Rishon LeZion, Israel.

ABSTRACT
When we contract an infection, we typically feel sick and behave accordingly. Symptoms of sickness behavior (SB) include anorexia, hypersomnia, depression, and reduced social interactions. SB affects species spanning from arthropods to vertebrates, is triggered nonspecifically by viruses, bacteria, and parasites, and is orchestrated by a complex network of cytokines and neuroendocrine pathways; clearly, it has been naturally selected. Nonetheless, SB seems evolutionarily costly: it promotes starvation and predation and reduces reproductive opportunities. How could SB persist? Former explanations focused on individual fitness, invoking improved resistance to pathogens. Could prevention of disease transmission, propagating in populations through kin selection, also contribute to SB?

No MeSH data available.


Related in: MedlinePlus

Information regarding inflammation is communicated to the brain through parallel neural and circulatory routes [4,5].Leukocytes, such as dendritic cells (DCs) and macrophages, sense microbes through pathogen-recognition receptors such as toll-like receptors (TLRs) and NOD-like receptors (NLRs) and then release inflammatory cytokines such as interleukin–1 beta (IL–1β), IL–6, and tumor necrosis factor alpha (TNF-α). In the neural route, cytokines trigger activity in vagal afferents that innervate nuclei in the brain stem such at the nucleus of the solitary tract (NTS). These in turn relay the signal to various nuclei in the hypothalamus, thalamus, and amygdala [4]. In the circulatory route, microbial ligands and cytokines travel through the blood to reach the meninges, choroid plexus, and circumventricular organs (pink) where they can enter the brain. More recent data indicate that such ligands can also activate the epithelium in areas with an intact blood–brain barrier, causing it to synthetize various prostaglandins and release them into nuclei involved in specific behaviors [6].
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4608734&req=5

pbio.1002276.g001: Information regarding inflammation is communicated to the brain through parallel neural and circulatory routes [4,5].Leukocytes, such as dendritic cells (DCs) and macrophages, sense microbes through pathogen-recognition receptors such as toll-like receptors (TLRs) and NOD-like receptors (NLRs) and then release inflammatory cytokines such as interleukin–1 beta (IL–1β), IL–6, and tumor necrosis factor alpha (TNF-α). In the neural route, cytokines trigger activity in vagal afferents that innervate nuclei in the brain stem such at the nucleus of the solitary tract (NTS). These in turn relay the signal to various nuclei in the hypothalamus, thalamus, and amygdala [4]. In the circulatory route, microbial ligands and cytokines travel through the blood to reach the meninges, choroid plexus, and circumventricular organs (pink) where they can enter the brain. More recent data indicate that such ligands can also activate the epithelium in areas with an intact blood–brain barrier, causing it to synthetize various prostaglandins and release them into nuclei involved in specific behaviors [6].

Mentions: A common misconception is that pathogens directly produce these behavioral symptoms, but in fact SB is orchestrated by the host’s immune and neuroendocrine systems; mammals have evolved several parallel pathways to alert the brain of inflammation and trigger symptomatic behaviors (Fig 1) [4,5].


Why Do We Feel Sick When Infected--Can Altruism Play a Role?

Shakhar K, Shakhar G - PLoS Biol. (2015)

Information regarding inflammation is communicated to the brain through parallel neural and circulatory routes [4,5].Leukocytes, such as dendritic cells (DCs) and macrophages, sense microbes through pathogen-recognition receptors such as toll-like receptors (TLRs) and NOD-like receptors (NLRs) and then release inflammatory cytokines such as interleukin–1 beta (IL–1β), IL–6, and tumor necrosis factor alpha (TNF-α). In the neural route, cytokines trigger activity in vagal afferents that innervate nuclei in the brain stem such at the nucleus of the solitary tract (NTS). These in turn relay the signal to various nuclei in the hypothalamus, thalamus, and amygdala [4]. In the circulatory route, microbial ligands and cytokines travel through the blood to reach the meninges, choroid plexus, and circumventricular organs (pink) where they can enter the brain. More recent data indicate that such ligands can also activate the epithelium in areas with an intact blood–brain barrier, causing it to synthetize various prostaglandins and release them into nuclei involved in specific behaviors [6].
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4608734&req=5

pbio.1002276.g001: Information regarding inflammation is communicated to the brain through parallel neural and circulatory routes [4,5].Leukocytes, such as dendritic cells (DCs) and macrophages, sense microbes through pathogen-recognition receptors such as toll-like receptors (TLRs) and NOD-like receptors (NLRs) and then release inflammatory cytokines such as interleukin–1 beta (IL–1β), IL–6, and tumor necrosis factor alpha (TNF-α). In the neural route, cytokines trigger activity in vagal afferents that innervate nuclei in the brain stem such at the nucleus of the solitary tract (NTS). These in turn relay the signal to various nuclei in the hypothalamus, thalamus, and amygdala [4]. In the circulatory route, microbial ligands and cytokines travel through the blood to reach the meninges, choroid plexus, and circumventricular organs (pink) where they can enter the brain. More recent data indicate that such ligands can also activate the epithelium in areas with an intact blood–brain barrier, causing it to synthetize various prostaglandins and release them into nuclei involved in specific behaviors [6].
Mentions: A common misconception is that pathogens directly produce these behavioral symptoms, but in fact SB is orchestrated by the host’s immune and neuroendocrine systems; mammals have evolved several parallel pathways to alert the brain of inflammation and trigger symptomatic behaviors (Fig 1) [4,5].

Bottom Line: Nonetheless, SB seems evolutionarily costly: it promotes starvation and predation and reduces reproductive opportunities.Former explanations focused on individual fitness, invoking improved resistance to pathogens.Could prevention of disease transmission, propagating in populations through kin selection, also contribute to SB?

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, College of Management Academic Studies, Rishon LeZion, Israel.

ABSTRACT
When we contract an infection, we typically feel sick and behave accordingly. Symptoms of sickness behavior (SB) include anorexia, hypersomnia, depression, and reduced social interactions. SB affects species spanning from arthropods to vertebrates, is triggered nonspecifically by viruses, bacteria, and parasites, and is orchestrated by a complex network of cytokines and neuroendocrine pathways; clearly, it has been naturally selected. Nonetheless, SB seems evolutionarily costly: it promotes starvation and predation and reduces reproductive opportunities. How could SB persist? Former explanations focused on individual fitness, invoking improved resistance to pathogens. Could prevention of disease transmission, propagating in populations through kin selection, also contribute to SB?

No MeSH data available.


Related in: MedlinePlus