scholarly journals Psychological Stress and the Cutaneous Immune Response: Roles of the HPA Axis and the Sympathetic Nervous System in Atopic Dermatitis and Psoriasis

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Jessica M. F. Hall ◽  
desAnges Cruser ◽  
Alan Podawiltz ◽  
Diana I. Mummert ◽  
Harlan Jones ◽  
...  

Psychological stress, an evolutionary adaptation to the fight-or-flight response, triggers a number of physiological responses that can be deleterious under some circumstances. Stress signals activate the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system. Elements derived from those systems (e.g., cortisol, catecholamines and neuropeptides) can impact the immune system and possible disease states. Skin provides a first line of defense against many environmental insults. A number of investigations have indicated that the skin is especially sensitive to psychological stress, and experimental evidence shows that the cutaneous innate and adaptive immune systems are affected by stressors. For example, psychological stress has been shown to reduce recovery time of the stratum corneum barrier after its removal (innate immunity) and alters antigen presentation by epidermal Langerhans cells (adaptive immunity). Moreover, psychological stress may trigger or exacerbate immune mediated dermatological disorders. Understanding how the activity of the psyche-nervous -immune system axis impinges on skin diseases may facilitate coordinated treatment strategies between dermatologists and psychiatrists. Herein, we will review the roles of the HPA axis and the sympathetic nervous system on the cutaneous immune response. We will selectively highlight how the interplay between psychological stress and the immune system affects atopic dermatitis and psoriasis.

1982 ◽  
Vol 242 (1) ◽  
pp. R30-R33 ◽  
Author(s):  
A. del Rey ◽  
H. O. Besedovsky ◽  
E. Sorkin ◽  
M. Da Prada ◽  
G. P. Bondiolotti

A quantitative relationship is reported between the magnitude of the immune response of rats to sheep red blood cells and diminution of splenic norepinephrine (NE). A decrease in concentration and content of NE in the spleen on day 3 after immunization was evident in both high- and low-responder animals, whereas a diminished concentration of NE persisted only in the high responders. This continuing NE diminution in high-responder animals is associated with increase in spleen weight, probably attributable to blood accumulation. These findings are consonant with the concept that the sympathetic nervous system is involved in immunoregulation.


1999 ◽  
Vol 13 (4) ◽  
pp. 271-278 ◽  
Author(s):  
Ewa Chelmicka Schorr ◽  
Barry G.W. Arnason

Author(s):  
Iñaki Robles-Vera ◽  
Marta Toral ◽  
Juan Duarte

Abstract There are numerous studies indicating a direct association between hypertension and gut microbiota in both animal models and humans. In this review, we focused on the imbalance in the gut microbiota composition relative to healthy state or homeostasis, termed dysbiosis, associated with hypertension and discuss the current knowledge regarding how microbiota regulates blood pressure (BP), involving the sympathetic nervous system and the immune system. The profile of ecological parameters and bacterial genera composition of gut dysbiosis in hypertension varies according to the experimental model of hypertension. Recent evidence supports that gut microbiota can protect or promote the development of hypertension by interacting with gut secondary lymph organs and altering T helper 17/regulatory T cells polarization, with subsequent changes in T cells infiltration in vascular tissues. Here, we also describe the bidirectional communication between the microbiome and the host via the sympathetic nervous system and its role in BP regulation. Dysbiosis in hypertension is mainly associated with reduced proportions of short-chain fatty acid-producing bacteria, mainly acetate- and butyrate-producing bacteria, and an increased enrichment of the genes for lipopolysaccharide biosynthesis and export, lending to moderate endotoxemia. The role of these metabolic and structural products in both immune and sympathetic system regulation and vascular inflammation was also analyzed. Overall, gut microbiota is now recognized as a well-established target to dietary interventions with prebiotics or probiotics to reduce BP.


2014 ◽  
Vol 2 (Suppl 1) ◽  
pp. O2
Author(s):  
M Kox ◽  
LT van Eijk ◽  
J Zwaag ◽  
J van den Wildenberg ◽  
FCJG Sweep ◽  
...  

1997 ◽  
Vol 12 (5) ◽  
pp. 225-238 ◽  
Author(s):  
David J. Torpy ◽  
George P. Chrousos Md

Critical illness leads to a coordinated reaction that is categorized as the stress response; activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system leads to metabolic and cardiovascular changes that are generally directed toward maintenance of homeostasis. The HPA axis and the sympathetic nervous system are linked via reciprocally activating brainstem pathways. The immune system acts via cytokines, which are hormones, to activate the HPA axis. Glucocorticoid secretion suppresses immune activity, thus completing an immune-HPA feedback loop. Restraint of immune activity may be a major function of glucocorticoids during stress, thus averting the potential for immune-mediated damage to healthy tissues. Cortisol also acts to produce adaptive metabolic, cardiovascular, and cognitive changes. Activation of the stress system is also associated with inhibition of thyroid, gonadal, and growth axes through neuroendocrine and peripheral mechanisms; such effects can be seen as directed toward conservation of energy. There is growing evidence that hyperfunction and hypofunction of the integrated stress system may lead to a variety of previously unexplained disorders. Recently, a more detailed understanding of the stress system combined with astute clinical observation of critically ill patients has led to promising new avenues for therapeutic investigation.


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