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Article: Sickness: From the focus on cytokines, prostaglandins, and complement factors to the perspectives of neurons

TitleSickness: From the focus on cytokines, prostaglandins, and complement factors to the perspectives of neurons
Authors
Issue Date2015
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neubiorev
Citation
Neuroscience & Biobehavioral Reviews, 2015, v. 57, p. 30-45 How to Cite?
AbstractSystemic inflammation leads to a variety of physiological (e.g. fever) and behavioral (e.g. anorexia, immobility, social withdrawal, depressed mood, disturbed sleep) responses that are collectively known as sickness. While these phenomena have been studied for the past few decades, the neurobiological mechanisms by which sickness occurs remain unclear. In this review, we first revisit how the body senses and responds to infections and injuries by eliciting systemic inflammation. Next, we focus on how peripheral inflammatory molecules such as cytokines, prostaglandins, and activated complement factors communicate with the brain to trigger neuroinflammation and sickness. Since depression also involves inflammation, we further elaborate on the interrelationship between sickness and depression. Finally, we discuss how immune activation can modulate neurons in the brain, and suggest future perspectives to help unravel how changes in neuronal functions relate to sickness responses.
Persistent Identifierhttp://hdl.handle.net/10722/218630
ISSN
2015 Impact Factor: 8.58
2015 SCImago Journal Rankings: 5.290

 

DC FieldValueLanguage
dc.contributor.authorPoon, DCH-
dc.contributor.authorHo, YS-
dc.contributor.authorChiu, K-
dc.contributor.authorWong, HL-
dc.contributor.authorChang, RCC-
dc.date.accessioned2015-09-18T06:48:42Z-
dc.date.available2015-09-18T06:48:42Z-
dc.date.issued2015-
dc.identifier.citationNeuroscience & Biobehavioral Reviews, 2015, v. 57, p. 30-45-
dc.identifier.issn0149-7634-
dc.identifier.urihttp://hdl.handle.net/10722/218630-
dc.description.abstractSystemic inflammation leads to a variety of physiological (e.g. fever) and behavioral (e.g. anorexia, immobility, social withdrawal, depressed mood, disturbed sleep) responses that are collectively known as sickness. While these phenomena have been studied for the past few decades, the neurobiological mechanisms by which sickness occurs remain unclear. In this review, we first revisit how the body senses and responds to infections and injuries by eliciting systemic inflammation. Next, we focus on how peripheral inflammatory molecules such as cytokines, prostaglandins, and activated complement factors communicate with the brain to trigger neuroinflammation and sickness. Since depression also involves inflammation, we further elaborate on the interrelationship between sickness and depression. Finally, we discuss how immune activation can modulate neurons in the brain, and suggest future perspectives to help unravel how changes in neuronal functions relate to sickness responses.-
dc.languageeng-
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neubiorev-
dc.relation.ispartofNeuroscience & Biobehavioral Reviews-
dc.titleSickness: From the focus on cytokines, prostaglandins, and complement factors to the perspectives of neurons-
dc.typeArticle-
dc.identifier.emailChiu, K: datwai@hkucc.hku.hk-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.authorityChiu, K=rp01973-
dc.identifier.authorityChang, RCC=rp00470-
dc.identifier.doi10.1016/j.neubiorev.2015.07.015-
dc.identifier.pmid26363665-
dc.identifier.hkuros251996-
dc.identifier.volume57-
dc.identifier.spage30-
dc.identifier.epage45-
dc.publisher.placeUnited Kingdom-

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