Background: Mental stress is believed to induce an exacerbation of atopic dermatitis (AD). Until now, however, only few psychoneuroendocrinologic mechanisms underlying the link between psychological stress and exacerbation or maintenance of AD have been described.
Objective: Our purpose was to conduct an investigation of immunologic parameters in the form of membrane molecules and cytokines with potential relevance for the cutaneous inflammation in an established psychological laboratory stress model.
Methods: Patients with AD (n = 15) and healthy controls (n = 15) were exposed to mental stress, as described in a previous report. In vitro analyses were completed 1 hour before, immediately after, and 1 hour after mental stress exposure. Lymphocyte subpopulations, the cutaneous lymphocyte-associated antigen (CLA), the membrane molecule CD69(+) (early activation antigen), and intracellular IL-4, IL-5, and IFN-gamma in blood-derived lymphocytes were analyzed by flow cytometry. IL-4 in the supernatant of concanavalin-A-stimulated PBMCs was determined by ELISA.
Results: An increase in heart rate and blood pressure was demonstrated during psychological stress in patients with AD and healthy volunteers. We found significantly higher stress-induced increase of CLA(+) lymphocytes, T helper cells expressing IL-5, and both CD4(+) and CD8(+) lymphocytes expressing IFN-gamma on mitogenic stimulation in patients with AD in comparison with healthy controls. In addition, we observed an earlier increase in the secretion of IL-4 in the supernatant of mitogen-stimulated lymphocytes during psychological stress in patients with AD in comparison with healthy volunteers.
Conclusion: A higher stress-induced increase of CLA(+) cells in the circulation in patients with AD compared to healthy controls might indicate an increased ability of T lymphocytes in AD to migrate to the skin during this psychological condition. In addition, the data of this study suggest a different stress-induced cytokine profile in circulating lymphocytes in patients with AD compared to healthy controls.