Catecholamines have a suppressive effect on cutaneous Langerhans cells, which anatomically are associated with cutaneous nerves. The bone marrow–derived Langerhans cells participate in the cutaneous immune response and migrate from skin to lymph nodes. They possess surface receptors common to macrophages and function as antigen-presenting cells to T or B lymphocytes.
The skin responds differently to acute versus chronic stress. Skin responses to acute stress include an enhanced skin immune function with increased intracutaneous migration of immunocompetent cells, while chronic stress may suppress cutaneous immunity. Lymphocytes express adrenergic receptors and respond to increased levels of catecholamines with the development of stress-induced lymphocytosis, changes in lymphocyte trafficking, circulation, proliferation, and cytokine production.
Acute stress experienced prior to the exposure to a novel antigen has been shown to increase memory T-cell formation, and acute stress experienced during antigen reexposure may enhance the secondary immune response. Alternatively, chronic stress may reduce the immune response to vaccines, slow wound healing (since the cellular immune response plays a key role in the early phase of wound healing), and reactivate latent viral infections such as herpesviruses.
Stress and the mast cell
Acute stress is associated with increased mast cell activation and degranulation.1 The mast cell is a key player in the skin-brain connection and an important regulator of neurogenic inflammation during the stress response. A wide range of stress-related mediators such as CRH, ACTH, cytokines, and substance P are triggers for mast cell activation, which, in turn, results in the synthesis and/or release of prestored mediators that may lead to the onset or exacerbation of a wide range of dermatologic disorders that are known to be exacerbated by psychological stress.
The skin mast cell is not only triggered by classic stress mediators such as ACTH and CRH, it is also a generator of stress hormones such as CRH. The skin mast cell is one of the richest sources of CRH outside the brain.1 Some of the dermatologic disorders in which mast cells play an important role include urticaria and angioedema, alopecia areata, atopic dermatitis, psoriasis, contact dermatitis, acne vulgaris, and various pruritic states that may be associated with mast cell activation and histamine release.
Acute psychological stress and skin barrier function
Some recent studies have demonstrated that acute psychological stress, which is associated with increased glucocorticoid levels, adversely affects skin barrier function recovery induced by tape stripping; in contrast, chronic psychological stress, which may be a feature of chronic posttraumatic stress disorder (PTSD), is often associated with an attenuated HPA axis response and has been associated with an enhancement in skin barrier function recovery. Glucocorticoids most likely act by inhibiting epidermal cell proliferation and lipid synthesis.
Psychodermatologic disorders have generally been classified into 2 major categories3:
- Cutaneous associations of psychiatric disorders.
- Psychiatric associations of cutaneous disorders.
Some of the dermatologic presentations of primary psychiatric symptoms are summarized in Table 1. The self-induced dermatoses represent the fact that stimulation of the skin, which is richly innervated and has bilateral communication with the CNS, serves as a means of regulating affect and coping with intense emotional states. In some instances the self-induced cutaneous lesions also communicate emotional distress.