Affiliations: Department of Psychology & Volen National Center for Complex Systems, Brandeis University, Waltham, MA, USA
Note: [] Correspondence to: Nicolas Rohleder, Assistant Professor, Department of Psychology & Volen National Center for Complex Systems, Brandeis University, 415 South Street, MS062 PO Box 549110, Waltham, MA 02454, USA. Tel.: +1 781 736 3319; Fax: +1 781 736 3291; E-mail: rohleder@brandeis.edu
Abstract: Chronic stress is an important predictor of morbidity and mortality in humans. While research has made major advances in understanding the biological pathways between long-term stress exposure and pathophysiological mechanisms underlying adverse health outcomes, one major issue remains: Alterations of major stress systems hypothalamus pituitary adrenal (HPA) axis and sympathetic nervous system (SNS) are not consistently found, and/or are insufficient in explaining the stress-disease link. Chronic, and systemic low-grade inflammation has emerged as a promising pathway, because inflammation is more consistently found elevated in conditions of chronic psychosocial stress, and these alterations of inflammatory activity can be directly related with specific pathophysiological mechanisms underlying important diseases associated with chronic stress, such as cardiovascular disease. However, increased inflammation is theoretically incompatible with the frequent finding of unchanged, or decreased basal HPA axis activity. It has therefore been suggested that one of the major changes in chronic stress manifests itself in the ability of the inflammatory tissues to adequately respond to anti-inflammatory signaling of stress systems. The aim of this review article is to summarize our current knowledge about the ability of the stress systems HPA axis, sympathetic, and parasympathetic nervous system to control inflammation.
