Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany
Atopic dermatitis (AD) is a chronic inflammatory skin disease
with the principal symptoms of dry skin, lichnification, eczematous
inflammation, and an intense pruritus. Despite general acceptance
that AD is a multifactorial skin disorder, dysregulation of
immune functions (e.g., hypersecretion of immunoglobulin-E,
altered cytokine profiles) is considered to be mainly involved
in AD pathogenesis. Considerable evidence points to an immunoregulatory
function for the hypothalamus-pituitary-adrenal (HPA) axis,
suggesting that appropriate reactivity of the HPA axis is necessary
to prevent the immune system from reaching a level that may
be damaging for the host. It is further hypothesized that dysfunctional
reactivity of the HPA axis may increase the vulnerability of
the organism to immune-related disorders such as inflammatory
diseases. In the present paper the role of the HPA axis for
the development and chronification of allergic inflammation
will be summarized and the potential pathological significance
of a dysfunctional HPA axis in AD pathogenesis will be discussed.
