A growing number of animal data strongly suggest that a hyporeactive hypothalamus-pituitary adrenal (HPA) axis may be pathologically significant by increasing the susceptibility to chronic inflammation. Following this line of evidence, the specific goal of the present study was to investigate the HPA axis in patients with atopic dermatitis (AD), a chronic allergic inflammatory disease. In addition, the sympathetic adrenomedullary (SAM) system as a second potent immunoregulatory and anti-inflammatory stress-response system has been examined. AD patients (n = 36) and nonatopic control subjects (n = 37) were exposed to a standardized laboratory stressor consisting of a free speech and mental arithmetic task in front of an audience. Cortisol, ACTH, and catecholamine concentrations were assessed before and after the stressor. To investigate feedback sensitivity of the HPA axis, a low dose (0.5 mg) dexamethasone suppression test was also performed. AD patients showed significantly attenuated cortisol and ACTH responses to the stressor, whereas catecholamine levels were significantly elevated in atopic patients. No difference between the experimental groups was found in basal cortisol and ACTH concentrations, whereas basal catecholamine levels were significantly elevated. Analysis of cortisol levels after dexamethasone treatment suggested an intact feedback sensitivity in AD sufferers at the pituitary level. The present findings suggest that patients with AD demonstrate a blunted HPA axis responsiveness with a concurrent overreactivity of the SAM system to psychosocial stress. Considering the important immunoregulatory role of the HPA axis and the SAM system, especially under stressful conditions, an aberrant responsiveness of these neuroendocrine systems may increase the susceptibility to (allergic) inflammation and may be one psychobiological mechanism of stress-related aggravation of the disease.

Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease with increasing incidence characterized by eczematous inflammation of the skin, a chronically relapsing course and severe pruritus. In the last decade, there has been growing evidence indicating that psychological factors such as personality and stress may play an important role in the pathogenesis of AD. While there is only little consensus on an AD-specific personality profile and its etiological significance, a growing number of reports support the role of psychosocial stress in the onset and the course of AD symptomatology. However, although a close association between psychosocial stress and skin condition in AD patients has been demonstrated by several investigators, pathological models that integrate stress and its effect on atopy-relevant biological processes, e.g. immune processes, are still missing. This overview summarizes the role of immunological and psychological factors in AD pathogenesis and discusses potential psychobiological pathways of stress-related modulation of AD symptoms.

Background: After primary orofacial infection with the herpes simplex virus (type 1, HSV-1), up to 40% of HSV seropositive subjects suffer recurrent herpes infections which are characterized by painful erosions of the involved skin mainly around the lips (herpes labialis). Besides various other factors, there is growing evidence suggesting that psychosocial factors might trigger HSV. The present study was designed to investigate modulation of recurrent HSV infection by experimentally induced emotional distress. Methods: Among patients with herpes labialis (n = 91), subjects who showed recurrent HSV infection (>5 acute infections/year) and who reported to suffer from HSV symptoms exclusively after confrontation with dirty dishes, i.e. dirty plates or dirty glasses were selected by standardized interview. Subjects (n = 20) were randomly assigned to two treatment groups. The experimental group (n = 10) was first exposed to 5 slides showing dirty glasses and subsequently to the glasses previously presented on the slides in vivo. The control group (n = 10) was exposed to neutral slides and neutral objects. In order to determine the proportion of leukocyte subpopulations and concentrations of tumor necrosis factor α (TNF-α), blood samples were collected 15 min before as well as 40 min and 48 h after stimulus presentation. Saliva cortisol was obtained 45, 20, 15 and 1 min before and 1, 10, 20 and 30 min after stimulus confrontation. Results: Medical examination of the volunteers 48 h after the experiment indicated that four experimental subjects showed HSV-1 symptoms while not a single herpetic infection could be determined in the control subjects (p = 0.033). Moreover, significantly elevated concentrations of TNF-α were observed in the experimental, but not in the control group. No significant alterations of the number of leukocyte subpopulations were found 30 min or 48 h after stimulus presentation. Further, cortisol concentrations were found to be unchanged after the treatment. Conclusions: The present findings suggest that experimentally induced emotional stress such as disgust may be associated with reactivation of HSV.