期刊论文详细信息
BMC Medicine
Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways
Brian Leonard5  Piotr Gałecki4  George Anderson1  Cai Song3  Lisa Goehler6  Michael Berk2  Michael Maes7 
[1]CRC, Rm 30, 57 Laurel street, Glasgow G11 7QT, Scotland, UK
[2]Department of Psychiatry, Melbourne University, Level 1, North Block Main Building Royal Melbourne Hospital, Parkville Victoria, 3050, Australia
[3]Department of Pharmacology, Chinese Academy Engineering Instit ute for the Development of Endangered Medicinal Resources in Southwest China 189 Changgang Road, Xing Ning District, Nanning, Guangxi Post Code 30023, P. R. China
[4]Department of Adult Psychiatry, Medical University of Łóź, Aleksandrowska 159, Łóź, 91-229, Poland
[5]Department of Pharmacology, Galway University, University Road, Galway, Co.Galway, Ireland
[6]Center for the Study of Complementary and Alternative Therapies, School of Nursing, University of Virginia, PO Box 800793, Charlottesville, VA 22908, USA
[7]Maes Clinics @ TRIA, Piyavate Hospital, 998 Rimklongsamsen Road, Bangkok 10310, Thailand
关键词: cytokines;    oxidative stress;    inflammation;    sickness behavior;    depression;   
Others  :  1126067
DOI  :  10.1186/1741-7015-10-66
 received in 2012-04-23, accepted in 2012-06-29,  发布年份 2012
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【 摘 要 】

It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.

【 授权许可】

   
2012 Maes et al; licensee BioMed Central Ltd.

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